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Boundless Biology: 37.3: Regulation of Body Processes

Boundless Biology
37.3: Regulation of Body Processes
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table of contents
  1. 1: The Study of Life
    1. 1.1: The Science of Biology
      1. 1.1.0: Introduction to the Study of Biology
      2. 1.1.1: Scientific Reasoning
      3. 1.1.2: The Scientific Method
      4. 1.1.3: Basic and Applied Science
      5. 1.1.4: Publishing Scientific Work
      6. 1.1.5: Branches and Subdisciplines of Biology
    2. 1.2: Themes and Concepts of Biology
      1. 1.2.0: Properties of Life
      2. 1.2.1: Levels of Organization of Living Things
      3. 1.2.2: The Diversity of Life
  2. 2: The Chemical Foundation of Life
    1. 2.1: Atoms, Isotopes, Ions, and Molecules
      1. 2.1.0: Overview of Atomic Structure
      2. 2.1.1: Atomic Number and Mass Number
      3. 2.1.2: Isotopes
      4. 2.1.3: The Periodic Table
      5. 2.1.4: Electron Shells and the Bohr Model
      6. 2.1.5: Electron Orbitals
      7. 2.1.6: Chemical Reactions and Molecules
      8. 2.1.7: Ions and Ionic Bonds
      9. 2.1.8: Covalent Bonds and Other Bonds and Interactions
      10. 2.1.9: Hydrogen Bonding and Van der Waals Forces
    2. 2.2: Water
      1. 2.2.0: Water’s Polarity
      2. 2.2.1: Water’s States: Gas, Liquid, and Solid
      3. 2.2.2: Water’s High Heat Capacity
      4. 2.2.3: Water’s Heat of Vaporization
      5. 2.2.4: Water’s Solvent Properties
      6. 2.2.5: Water’s Cohesive and Adhesive Properties
      7. 2.2.6: pH, Buffers, Acids, and Bases
    3. 2.3: Carbon
      1. 2.3.0: The Chemical Basis for Life
      2. 2.3.1: Hydrocarbons
      3. 2.3.2: Organic Isomers
      4. 2.3.3: Organic Enantiomers
      5. 2.3.4: Organic Molecules and Functional Groups
  3. 3: Biological Macromolecules
    1. 3.1: Synthesis of Biological Macromolecules
      1. 3.1.0: Types of Biological Macromolecules
      2. 3.1.1: Dehydration Synthesis
      3. 3.1.2: Hydrolysis
    2. 3.2: Carbohydrates
      1. 3.2.0: Carbohydrate Molecules
      2. 3.2.1: Importance of Carbohydrates
    3. 3.3: Lipids
      1. 3.3.0: Lipid Molecules
      2. 3.3.1: Waxes
      3. 3.3.2: Phospholipids
      4. 3.3.3: Steroids
    4. 3.4: Proteins
      1. 3.4.0: Types and Functions of Proteins
      2. 3.4.1: Amino Acids
      3. 3.4.2: Protein Structure
      4. 3.4.3: Denaturation and Protein Folding
    5. 3.5: Nucleic Acids
      1. 3.5.0: DNA and RNA
      2. 3.5.1: The DNA Double Helix
      3. 3.5.2: DNA Packaging
      4. 3.5.3: Types of RNA
  4. 4: Cell Structure
    1. 4.1: Studying Cells
      1. 4.1.0: Cells as the Basic Unit of Life
      2. 4.1.1: Microscopy
      3. 4.1.2: Cell Theory
      4. 4.1.3: Cell Size
    2. 4.2: Prokaryotic Cells
      1. 4.2.0: Characteristics of Prokaryotic Cells
    3. 4.3: Eukaryotic Cells
      1. 4.3.0: Characteristics of Eukaryotic Cells
      2. 4.3.1: The Plasma Membrane and the Cytoplasm
      3. 4.3.2: The Nucleus and Ribosomes
      4. 4.3.3: Mitochondria
      5. 4.3.4: Comparing Plant and Animal Cells
    4. 4.4: The Endomembrane System and Proteins
      1. 4.4.0: Vesicles and Vacuoles
      2. 4.4.1: The Endoplasmic Reticulum
      3. 4.4.2: The Golgi Apparatus
      4. 4.4.3: Lysosomes
      5. 4.4.4: Peroxisomes
    5. 4.5: The Cytoskeleton
      1. 4.5.0: Microfilaments
      2. 4.5.1: Intermediate Filaments and Microtubules
    6. 4.6: Connections between Cells and Cellular Activities
      1. 4.6.0: Extracellular Matrix of Animal Cells
      2. 4.6.1: Intercellular Junctions
  5. 5: Structure and Function of Plasma Membranes
    1. 5.1: Components and Structure
      1. 5.1.0: Components of Plasma Membranes
      2. 5.1.1: Fluid Mosaic Model
      3. 5.1.2: Membrane Fluidity
    2. 5.2: Passive Transport
      1. 5.2.0: The Role of Passive Transport
      2. 5.2.1: Selective Permeability
      3. 5.2.2: Diffusion
      4. 5.2.3: Facilitated transport
      5. 5.2.4: Osmosis
      6. 5.2.5: Tonicity
      7. 5.2.6: Osmoregulation
    3. 5.3: Active Transport
      1. 5.3.0: Electrochemical Gradient
      2. 5.3.1: Primary Active Transport
      3. 5.3.2: Secondary Active Transport
    4. 5.4: Bulk Transport
      1. 5.4.0: Endocytosis
      2. 5.4.1: Exocytosis
  6. 6: Metabolism
    1. 6.1: Energy and Metabolism
      1. 6.1.0: The Role of Energy and Metabolism
      2. 6.1.1: Types of Energy
      3. 6.1.2: Metabolic Pathways
      4. 6.1.3: Metabolism of Carbohydrates
    2. 6.2: Potential, Kinetic, Free, and Activation Energy
      1. 6.2.0: Free Energy
      2. 6.2.1: The First Law of Thermodynamics
      3. 6.2.2: The Second Law of Thermodynamics
      4. 6.2.3: Activation Energy
    3. 6.3: ATP: Adenosine Triphosphate
      1. 6.3.0: ATP: Adenosine Triphosphate
    4. 6.4: Enzymes
      1. 6.4.0: Enzyme Active Site and Substrate Specificity
      2. 6.4.1: Control of Metabolism Through Enzyme Regulation
  7. 7: Cellular Respiration
    1. 7.1: Energy in Living Systems
      1. 7.1.0: Transforming Chemical Energy
      2. 7.1.1: Electrons and Energy
      3. 7.1.2: ATP in Metabolism
    2. 7.2: Glycolysis
      1. 7.2.0: Importance of Glycolysis
      2. 7.2.1: The Energy-Requiring Steps of Glycolysis
      3. 7.2.2: The Energy-Releasing Steps of Glycolysis
      4. 7.2.3: Outcomes of Glycolysis
    3. 7.3: Oxidation of Pyruvate and the Citric Acid Cycle
      1. 7.3.0: Breakdown of Pyruvate
      2. 7.3.1: Acetyl CoA to CO2
      3. 7.3.2: Citric Acid Cycle
    4. 7.4: Oxidative Phosphorylation
      1. 7.4.0: Electron Transport Chain
      2. 7.4.1: Chemiosmosis and Oxidative Phosphorylation
      3. 7.4.2: ATP Yield
    5. 7.5: Metabolism without Oxygen
      1. 7.5.0: Anaerobic Cellular Respiration
    6. 7.6: Connections of Carbohydrate, Protein, and Lipid Metabolic Pathways
      1. 7.6.0: Connecting Other Sugars to Glucose Metabolism
      2. 7.6.1: Connecting Proteins to Glucose Metabolism
      3. 7.6.2: Connecting Lipids to Glucose Metabolism
    7. 7.7: Regulation of Cellular Respiration
      1. 7.7.0: Regulatory Mechanisms for Cellular Respiration
      2. 7.7.1: Control of Catabolic Pathways
  8. 8: Photosynthesis
    1. 8.1: Overview of Photosynthesis
      1. 8.1.0: The Purpose and Process of Photosynthesis
      2. 8.1.1: Main Structures and Summary of Photosynthesis
      3. 8.1.2: The Two Parts of Photosynthesis
    2. 8.2: The Light-Dependent Reactions of Photosynthesis
      1. 8.2.0: Introduction to Light Energy
      2. 8.2.1: Absorption of Light
      3. 8.2.2: Processes of the Light-Dependent Reactions
    3. 8.3: The Light-Independent Reactions of Photosynthesis
      1. 8.3.0: CAM and C4 Photosynthesis
      2. 8.3.1: The Calvin Cycle
      3. 8.3.2: The Carbon Cycle
  9. 9: Cell Communication
    1. 9.1: Signaling Molecules and Cellular Receptors
      1. 9.1.0: Signaling Molecules and Cellular Receptors
      2. 9.1.1: Forms of Signaling
      3. 9.1.2: Types of Receptors
      4. 9.1.3: Signaling Molecules
    2. 9.2: Propagation of the Cellular Signal
      1. 9.2.0: Binding Initiates a Signaling Pathway
      2. 9.2.1: Methods of Intracellular Signaling
    3. 9.3: Response to the Cellular Signal
      1. 9.3.0: Termination of the Signal Cascade
      2. 9.3.1: Cell Signaling and Gene Expression
      3. 9.3.2: Cell Signaling and Cellular Metabolism
      4. 9.3.3: Cell Signaling and Cell Growth
      5. 9.3.4: Cell Signaling and Cell Death
    4. 9.4: Signaling in Single-Celled Organisms
      1. 9.4.0: Signaling in Yeast
      2. 9.4.1: Signaling in Bacteria
  10. 10: Cell Reproduction
    1. 10.1: Cell Division
      1. 10.1.0: The Role of the Cell Cycle
      2. 10.1.1: Genomic DNA and Chromosomes
      3. 10.1.2: Eukaryotic Chromosomal Structure and Compaction
    2. 10.2: The Cell Cycle
      1. 10.2.0: Interphase
      2. 10.2.1: The Mitotic Phase and the G0 Phase
    3. 10.3: Control of the Cell Cycle
      1. 10.3.0: Regulation of the Cell Cycle by External Events
      2. 10.3.1: Regulation of the Cell Cycle at Internal Checkpoints
      3. 10.3.2: Regulator Molecules of the Cell Cycle
    4. 10.4: Cancer and the Cell Cycle
      1. 10.4.0: Proto-oncogenes
      2. 10.4.1: Tumor Suppressor Genes
    5. 10.5: Prokaryotic Cell Division
      1. 10.5.0: Binary Fission
  11. 11: Meiosis and Sexual Reproduction
    1. 11.1: The Process of Meiosis
      1. 11.1.0: Introduction to Meiosis
      2. 11.1.1: Meiosis I
      3. 11.1.2: Meiosis II
      4. 11.1.3: Comparing Meiosis and Mitosis
    2. 11.2: Sexual Reproduction
      1. 11.2.0: Advantages and Disadvantages of Sexual Reproduction
      2. 11.2.1: Life Cycles of Sexually Reproducing Organisms
  12. 12: Mendel's Experiments and Heredity
    1. 12.1: Mendel’s Experiments and the Laws of Probability
      1. 12.1.0: Introduction to Mendelian Inheritance
      2. 12.1.1: Mendel’s Model System
      3. 12.1.2: Mendelian Crosses
      4. 12.1.3: Garden Pea Characteristics Revealed the Basics of Heredity
      5. 12.1.4: Rules of Probability for Mendelian Inheritance
    2. 12.2: Patterns of Inheritance
      1. 12.2.0: Genes as the Unit of Heredity
      2. 12.2.1: Phenotypes and Genotypes
      3. 12.2.2: The Punnett Square Approach for a Monohybrid Cross
      4. 12.2.3: Alternatives to Dominance and Recessiveness
      5. 12.2.4: Sex-Linked Traits
      6. 12.2.5: Lethal Inheritance Patterns
    3. 12.3: Laws of Inheritance
      1. 12.3.0: Mendel's Laws of Heredity
      2. 12.3.1: Mendel's Law of Dominance
      3. 12.3.2: Mendel's Law of Segregation
      4. 12.3.3: Mendel's Law of Independent Assortment
      5. 12.3.4: Genetic Linkage and Violation of the Law of Independent Assortment
      6. 12.3.5: Epistasis
  13. 13: Modern Understandings of Inheritance
    1. 13.1: Chromosomal Theory and Genetic Linkage
      1. 13.1.0: Chromosomal Theory of Inheritance
      2. 13.1.1: Genetic Linkage and Distances
      3. 13.1.2: Identification of Chromosomes and Karyotypes
    2. 13.2: Chromosomal Basis of Inherited Disorders
      1. 13.2.0: Disorders in Chromosome Number
      2. 13.2.1: Chromosomal Structural Rearrangements
      3. 13.2.2: X-Inactivation
  14. 14: DNA Structure and Function
    1. 14.1: Historical Basis of Modern Understanding
      1. 14.1.0: Discovery of DNA
      2. 14.1.1: Modern Applications of DNA
    2. 14.2: DNA Structure and Sequencing
      1. 14.2.0: The Structure and Sequence of DNA
      2. 14.2.1: DNA Sequencing Techniques
    3. 14.3: DNA Replication
      1. 14.3.0: Basics of DNA Replication
      2. 14.3.1: DNA Replication in Prokaryotes
      3. 14.3.2: DNA Replication in Eukaryotes
      4. 14.3.3: Telomere Replication
    4. 14.4: DNA Repair
      1. 14.4.0: DNA Repair
  15. 15: Genes and Proteins
    1. 15.1: The Genetic Code
      1. 15.1.0: The Relationship Between Genes and Proteins
      2. 15.1.1: The Central Dogma: DNA Encodes RNA and RNA Encodes Protein
    2. 15.2: Prokaryotic Transcription
      1. 15.2.0: Transcription in Prokaryotes
      2. 15.2.1: Initiation of Transcription in Prokaryotes
      3. 15.2.2: Elongation and Termination in Prokaryotes
    3. 15.3: Eukaryotic Transcription
      1. 15.3.0: Initiation of Transcription in Eukaryotes
      2. 15.3.1: Elongation and Termination in Eukaryotes
    4. 15.4: RNA Processing in Eukaryotes
      1. 15.4.0: mRNA Processing
      2. 15.4.1: Processing of tRNAs and rRNAs
    5. 15.5: Ribosomes and Protein Synthesis
      1. 15.5.0: The Protein Synthesis Machinery
      2. 15.5.1: The Mechanism of Protein Synthesis
      3. 15.5.2: Protein Folding, Modification, and Targeting
  16. 16: Gene Expression
    1. 16.1: Regulation of Gene Expression
      1. 16.1.0: The Process and Purpose of Gene Expression Regulation
      2. 16.1.1: Prokaryotic versus Eukaryotic Gene Expression
    2. 16.2: Prokaryotic Gene Regulation
      1. 16.2.0: The trp Operon: A Repressor Operon
      2. 16.2.1: Catabolite Activator Protein (CAP): An Activator Regulator
      3. 16.2.2: The lac Operon: An Inducer Operon
    3. 16.3: Eukaryotic Gene Regulation
      1. 16.3.0: The Promoter and the Transcription Machinery
      2. 16.3.1: Transcriptional Enhancers and Repressors
      3. 16.3.2: Epigenetic Control: Regulating Access to Genes within the Chromosome
      4. 16.3.3: RNA Splicing
      5. 16.3.4: The Initiation Complex and Translation Rate
      6. 16.3.5: Regulating Protein Activity and Longevity
    4. 16.4: Regulating Gene Expression in Cell Development
      1. 16.4.0: Gene Expression in Stem Cells
      2. 16.4.1: Cellular Differentiation
      3. 16.4.2: Mechanics of Cellular Differentation
      4. 16.4.3: Establishing Body Axes during Development
      5. 16.4.4: Gene Expression for Spatial Positioning
      6. 16.4.5: Cell Migration in Multicellular Organisms
      7. 16.4.6: Programmed Cell Death
    5. 16.5: Cancer and Gene Regulation
      1. 16.5.0: Altered Gene Expression in Cancer
      2. 16.5.1: Epigenetic Alterations in Cancer
      3. 16.5.2: Cancer and Transcriptional Control
      4. 16.5.3: Cancer and Post-Transcriptional Control
      5. 16.5.4: Cancer and Translational Control
  17. 17: Biotechnology and Genomics
    1. 17.1: Biotechnology
      1. 17.1.0: Biotechnology
      2. 17.1.1: Basic Techniques to Manipulate Genetic Material (DNA and RNA)
      3. 17.1.2: Molecular and Cellular Cloning
      4. 17.1.3: Reproductive Cloning
      5. 17.1.4: Genetic Engineering
      6. 17.1.5: Genetically Modified Organisms (GMOs)
      7. 17.1.6: Biotechnology in Medicine
      8. 17.1.7: Production of Vaccines, Antibiotics, and Hormones
    2. 17.2: Mapping Genomes
      1. 17.2.0: Genetic Maps
      2. 17.2.1: Physical Maps and Integration with Genetic Maps
    3. 17.3: Whole-Genome Sequencing
      1. 17.3.0: Strategies Used in Sequencing Projects
      2. 17.3.1: Use of Whole-Genome Sequences of Model Organisms
      3. 17.3.2: Uses of Genome Sequences
    4. 17.4: Applying Genomics
      1. 17.4.0: Predicting Disease Risk at the Individual Level
      2. 17.4.1: Pharmacogenomics, Toxicogenomics, and Metagenomics
      3. 17.4.2: Genomics and Biofuels
    5. 17.5: Genomics and Proteomics
      1. 17.5.0: Genomics and Proteomics
      2. 17.5.1: Basic Techniques in Protein Analysis
      3. 17.5.2: Cancer Proteomics
  18. 18: Evolution and the Origin of Species
    1. 18.1: Understanding Evolution
      1. 18.1.0: What is Evolution?
      2. 18.1.1: Charles Darwin and Natural Selection
      3. 18.1.2: The Galapagos Finches and Natural Selection
      4. 18.1.3: Processes and Patterns of Evolution
      5. 18.1.4: Evidence of Evolution
      6. 18.1.5: Misconceptions of Evolution
    2. 18.2: Formation of New Species
      1. 18.2.0: The Biological Species Concept
      2. 18.2.1: Reproductive Isolation
      3. 18.2.2: Speciation
      4. 18.2.3: Allopatric Speciation
      5. 18.2.4: Sympatric Speciation
    3. 18.3: Hybrid Zones and Rates of Speciation
      1. 18.3.0: Hybrid Zones
      2. 18.3.1: Varying Rates of Speciation
    4. 18.4: Evolution of Genomes
      1. 18.4.0: Genomic Similiarities between Distant Species
      2. 18.4.1: Genome Evolution
      3. 18.4.2: Whole-Genome Duplication
      4. 18.4.3: Gene Duplications and Divergence
      5. 18.4.4: Noncoding DNA
      6. 18.4.5: Variations in Size and Number of Genes
    5. 18.5: Evidence of Evolution
      1. 18.5.0: The Fossil Record as Evidence for Evolution
      2. 18.5.1: Fossil Formation
      3. 18.5.2: Gaps in the Fossil Record
      4. 18.5.3: Carbon Dating and Estimating Fossil Age
      5. 18.5.4: The Fossil Record and the Evolution of the Modern Horse
      6. 18.5.5: Homologous Structures
      7. 18.5.6: Convergent Evolution
      8. 18.5.7: Vestigial Structures
      9. 18.5.8: Biogeography and the Distribution of Species
  19. 19: The Evolution of Populations
    1. 19.1: Population Evolution
      1. 19.1.0: Defining Population Evolution
      2. 19.1.1: Population Genetics
      3. 19.1.2: Hardy-Weinberg Principle of Equilibrium
    2. 19.2: Population Genetics
      1. 19.2.0: Genetic Variation
      2. 19.2.1: Genetic Drift
      3. 19.2.2: Gene Flow and Mutation
      4. 19.2.3: Nonrandom Mating and Environmental Variance
    3. 19.3: Adaptive Evolution
      1. 19.3.0: Natural Selection and Adaptive Evolution
      2. 19.3.1: Stabilizing, Directional, and Diversifying Selection
      3. 19.3.2: Frequency-Dependent Selection
      4. 19.3.3: Sexual Selection
      5. 19.3.4: No Perfect Organism
  20. 20: Phylogenies and the History of Life
    1. 20.1: Organizing Life on Earth
      1. 20.1.0: Phylogenetic Trees
      2. 20.1.1: Limitations of Phylogenetic Trees
      3. 20.1.2: The Levels of Classification
    2. 20.2: Determining Evolutionary Relationships
      1. 20.2.0: Distinguishing between Similar Traits
      2. 20.2.1: Building Phylogenetic Trees
    3. 20.3: Perspectives on the Phylogenetic Tree
      1. 20.3.0: Limitations to the Classic Model of Phylogenetic Trees
      2. 20.3.1: Horizontal Gene Transfer
      3. 20.3.2: Endosymbiotic Theory and the Evolution of Eukaryotes
      4. 20.3.3: Web, Network, and Ring of Life Models
  21. 21: Viruses
    1. 21.1: Viral Evolution, Morphology, and Classification
      1. 21.1.0: Discovery and Detection of Viruses
      2. 21.1.1: Evolution of Viruses
      3. 21.1.2: Viral Morphology
      4. 21.1.3: Virus Classification
    2. 21.2: Virus Infections and Hosts
      1. 21.2.0: Steps of Virus Infections
      2. 21.2.1: The Lytic and Lysogenic Cycles of Bacteriophages
      3. 21.2.2: Animal Viruses
      4. 21.2.3: Plant Viruses
    3. 21.3: Prevention and Treatment of Viral Infections
      1. 21.3.0: Vaccines and Immunity
      2. 21.3.1: Vaccines and Anti-Viral Drugs for Treatment
    4. 21.4: Prions and Viroids
      1. 21.4.0: Prions and Viroids
  22. 22: Prokaryotes: Bacteria and Archaea
    1. 22.1: Prokaryotic Diversity
      1. 22.1.0: Classification of Prokaryotes
      2. 22.1.1: The Origins of Archaea and Bacteria
      3. 22.1.2: Extremophiles and Biofilms
    2. 22.2: Structure of Prokaryotes
      1. 22.2.0: Basic Structures of Prokaryotic Cells
      2. 22.2.1: Prokaryotic Reproduction
    3. 22.3: Prokaryotic Metabolism
      1. 22.3.0: Energy and Nutrient Requirements for Prokaryotes
      2. 22.3.1: The Role of Prokaryotes in Ecosystems
    4. 22.4: Bacterial Diseases in Humans
      1. 22.4.0: History of Bacterial Diseases
      2. 22.4.1: Biofilms and Disease
      3. 22.4.2: Antibiotics: Are We Facing a Crisis?
      4. 22.4.3: Bacterial Foodborne Diseases
    5. 22.5: Beneficial Prokaryotes
      1. 22.5.0: Symbiosis between Bacteria and Eukaryotes
      2. 22.5.1: Early Biotechnology: Cheese, Bread, Wine, Beer, and Yogurt
      3. 22.5.2: Prokaryotes and Environmental Bioremediation
  23. 23: Protists
    1. 23.1: Eukaryotic Origins
      1. 23.1.0: Early Eukaryotes
      2. 23.1.1: Characteristics of Eukaryotic DNA
      3. 23.1.2: Endosymbiosis and the Evolution of Eukaryotes
      4. 23.1.3: The Evolution of Mitochondria
      5. 23.1.4: The Evolution of Plastids
    2. 23.2: Characteristics of Protists
      1. 23.2.0: Cell Structure, Metabolism, and Motility
      2. 23.2.1: Protist Life Cycles and Habitats
    3. 23.3: Groups of Protists
      1. 23.3.0: Excavata
      2. 23.3.1: Chromalveolata: Alveolates
      3. 23.3.2: Chromalveolata: Stramenopiles
      4. 23.3.3: Rhizaria
      5. 23.3.4: Archaeplastida
      6. 23.3.5: Amoebozoa and Opisthokonta
    4. 23.4: Ecology of Protists
      1. 23.4.0: Protists as Primary Producers, Food Sources, and Symbionts
      2. 23.4.1: Protists as Human Pathogens
      3. 23.4.2: Protists as Plant Pathogens
  24. 24: Fungi
    1. 24.1: Characteristics of Fungi
      1. 24.1.0: Characteristics of Fungi
      2. 24.1.1: Fungi Cell Structure and Function
      3. 24.1.2: Fungi Reproduction
    2. 24.2: Ecology of Fungi
      1. 24.2.0: Fungi Habitat, Decomposition, and Recycling
      2. 24.2.1: Mutualistic Relationships with Fungi and Fungivores
    3. 24.3: Classifications of Fungi
      1. 24.3.0: Chytridiomycota: The Chytrids
      2. 24.3.1: Zygomycota: The Conjugated Fungi
      3. 24.3.2: Ascomycota: The Sac Fungi
      4. 24.3.3: Basidiomycota: The Club Fungi
      5. 24.3.4: Deuteromycota: The Imperfect Fungi
      6. 24.3.5: Glomeromycota
    4. 24.4: Fungal Parasites and Pathogens
      1. 24.4.0: Fungi as Plant, Animal, and Human Pathogens
    5. 24.5: Importance of Fungi in Human Life
      1. 24.5.0: Importance of Fungi in Human Life
  25. 25: Seedless Plants
    1. 25.1: Early Plant Life
      1. 25.1.0: Early Plant Life
      2. 25.1.1: Evolution of Land Plants
      3. 25.1.2: Plant Adaptations to Life on Land
      4. 25.1.3: Sporophytes and Gametophytes in Seedless Plants
      5. 25.1.4: Structural Adaptations for Land in Seedless Plants
      6. 25.1.5: The Major Divisions of Land Plants
    2. 25.2: Green Algae: Precursors of Land Plants
      1. 25.2.0: Streptophytes and Reproduction of Green Algae
      2. 25.2.1: Charales
    3. 25.3: Bryophytes
      1. 25.3.0: Bryophytes
      2. 25.3.1: Liverworts and Hornworts
      3. 25.3.2: Mosses
    4. 25.4: Seedless Vascular Plants
      1. 25.4.0: Seedless Vascular Plants
      2. 25.4.1: Vascular Tissue: Xylem and Phloem
      3. 25.4.2: The Evolution of Roots in Seedless Plants
      4. 25.4.3: Ferns and Other Seedless Vascular Plants
      5. 25.4.4: The Importance of Seedless Vascular Plants
  26. 26: Seed Plants
    1. 26.1: Evolution of Seed Plants
      1. 26.1.0: The Evolution of Seed Plants and Adaptations for Land
      2. 26.1.1: Evolution of Gymnosperms
      3. 26.1.2: Evolution of Angiosperms
    2. 26.2: Gymnosperms
      1. 26.2.0: Characteristics of Gymnosperms
      2. 26.2.1: Life Cycle of a Conifer
      3. 26.2.2: Diversity of Gymnosperms
    3. 26.3: Angiosperms
      1. 26.3.0: Angiosperm Flowers
      2. 26.3.1: Angsiosperm Fruit
      3. 26.3.2: The Life Cycle of an Angiosperm
      4. 26.3.3: Diversity of Angiosperms
    4. 26.4: The Role of Seed Plants
      1. 26.4.0: Herbivory and Pollination
      2. 26.4.1: The Importance of Seed Plants in Human Life
      3. 26.4.2: Biodiversity of Plants
  27. 27: Introduction to Animal Diversity
    1. 27.1: Features of the Animal Kingdom
      1. 27.1.0: Characteristics of the Animal Kingdom
      2. 27.1.1: Complex Tissue Structure
      3. 27.1.2: Animal Reproduction and Development
    2. 27.2: Features Used to Classify Animals
      1. 27.2.0: Animal Characterization Based on Body Symmetry
      2. 27.2.1: Animal Characterization Based on Features of Embryological Development
    3. 27.3: Animal Phylogeny
      1. 27.3.0: Constructing an Animal Phylogenetic Tree
      2. 27.3.1: Molecular Analyses and Modern Phylogenetic Trees
    4. 27.4: The Evolutionary History of the Animal Kingdom
      1. 27.4.0: Pre-Cambrian Animal Life
      2. 27.4.1: The Cambrian Explosion of Animal Life
      3. 27.4.2: Post-Cambrian Evolution and Mass Extinctions
  28. 28: Invertebrates
    1. 28.1: Phylum Porifera
      1. 28.1.0: Phylum Porifera
      2. 28.1.1: Morphology of Sponges
      3. 28.1.2: Physiological Processes in Sponges
    2. 28.2: Phylum Cnidaria
      1. 28.2.0: Phylum Cnidaria
      2. 28.2.1: Class Anthozoa
      3. 28.2.2: Class Scyphozoa
      4. 28.2.3: Class Cubozoa and Class Hydrozoa
    3. 28.3: Superphylum Lophotrochozoa
      1. 28.3.0: Superphylum Lophotrochozoa
      2. 28.3.1: Phylum Platyhelminthes
      3. 28.3.2: Phylum Rotifera
      4. 28.3.3: Phylum Nemertea
      5. 28.3.4: Phylum Mollusca
      6. 28.3.5: Classification of Phylum Mollusca
      7. 28.3.6: Phylum Annelida
    4. 28.4: Superphylum Ecdysozoa
      1. 28.4.0: Superphylum Ecdysozoa
      2. 28.4.1: Phylum Nematoda
      3. 28.4.2: Phylum Arthropoda
      4. 28.4.3: Subphyla of Arthropoda
    5. 28.5: Superphylum Deuterostomia
      1. 28.5.0: Phylum Echinodermata
      2. 28.5.1: Classes of Echinoderms
      3. 28.5.2: Phylum Chordata
  29. 29: Vertebrates
    1. 29.1: Chordates
      1. 29.1.0: Characteristics of Chordata
      2. 29.1.1: Chordates and the Evolution of Vertebrates
      3. 29.1.2: The Evolution of Craniata and Vertebrata
      4. 29.1.3: Characteristics of Vertebrates
    2. 29.2: Fishes
      1. 29.2.0: Agnathans: Jawless Fishes
      2. 29.2.1: Gnathostomes: Jawed Fishes
    3. 29.3: Amphibians
      1. 29.3.0: Characteristics and Evolution of Amphibians
      2. 29.3.1: Modern Amphibians
    4. 29.4: Reptiles
      1. 29.4.0: Characteristics of Amniotes
      2. 29.4.1: Evolution of Amniotes
      3. 29.4.2: Characteristics of Reptiles
      4. 29.4.3: Evolution of Reptiles
      5. 29.4.4: Modern Reptiles
    5. 29.5: Birds
      1. 29.5.0: Characteristics of Birds
      2. 29.5.1: Evolution of Birds
    6. 29.6: Mammals
      1. 29.6.0: Characteristics of Mammals
      2. 29.6.1: Evolution of Mammals
      3. 29.6.2: Living Mammals
    7. 29.7: The Evolution of Primates
      1. 29.7.0: Characteristics and Evolution of Primates
      2. 29.7.1: Early Human Evolution
      3. 29.7.2: Early Hominins
      4. 29.7.3: Genus Homo
  30. 30: Plant Form and Physiology
    1. 30.1: The Plant Body
      1. 30.1.0: Plant Tissues and Organ Systems
    2. 30.2: Stems
      1. 30.2.0: Functions of Stems
      2. 30.2.1: Stem Anatomy
      3. 30.2.2: Primary and Secondary Growth in Stems
      4. 30.2.3: Stem Modifications
    3. 30.3: Roots
      1. 30.3.0: Types of Root Systems and Zones of Growth
      2. 30.3.1: Root Modifications
    4. 30.4: Leaves
      1. 30.4.0: Leaf Structure and Arrangment
      2. 30.4.1: Types of Leaf Forms
      3. 30.4.2: Leaf Structure, Function, and Adaptation
    5. 30.5: Plant Development
      1. 30.5.0: Meristems
      2. 30.5.1: Genetic Control of Flowers
    6. 30.6: Transport of Water and Solutes in Plants
      1. 30.6.0: Water and Solute Potential
      2. 30.6.1: Pressure, Gravity, and Matric Potential
      3. 30.6.2: Movement of Water and Minerals in the Xylem
      4. 30.6.3: Transportation of Photosynthates in the Phloem
    7. 30.7: Plant Sensory Systems and Responses
      1. 30.7.0: Plant Responses to Light
      2. 30.7.1: The Phytochrome System and Red Light Response
      3. 30.7.2: Blue Light Response
      4. 30.7.3: Plant Responses to Gravity
      5. 30.7.4: Auxins, Cytokinins, and Gibberellins
      6. 30.7.5: Abscisic Acid, Ethylene, and Nontraditional Hormones
      7. 30.7.6: Plant Responses to Wind and Touch
    8. 30.8: Plant Defense Mechanisms
      1. 30.8.0: Plant Defenses Against Herbivores
      2. 30.8.1: Plant Defenses Against Pathogens
  31. 31: Soil and Plant Nutrition
    1. 31.1: Nutritional Requirements of Plants
      1. 31.1.0: Plant Nutrition
      2. 31.1.1: The Chemical Composition of Plants
      3. 31.1.2: Essential Nutrients for Plants
    2. 31.2: The Soil
      1. 31.2.0: Soil Composition
      2. 31.2.1: Soil Formation
      3. 31.2.2: Physical Properties of Soil
    3. 31.3: Nutritional Adaptations of Plants
      1. 31.3.0: Nitrogen Fixation: Root and Bacteria Interactions
      2. 31.3.1: Mycorrhizae: The Symbiotic Relationship between Fungi and Roots
      3. 31.3.2: Nutrients from Other Sources
  32. 32: Plant Reproduction
    1. 32.1: Plant Reproductive Development and Structure
      1. 32.1.0: Plant Reproductive Development and Structure
      2. 32.1.1: Sexual Reproduction in Gymnosperms
      3. 32.1.2: Sexual Reproduction in Angiosperms
    2. 32.2: Pollination and Fertilization
      1. 32.2.0: Pollination and Fertilization
      2. 32.2.1: Pollination by Insects
      3. 32.2.2: Pollination by Bats, Birds, Wind, and Water
      4. 32.2.3: Double Fertilization in Plants
      5. 32.2.4: Development of the Seed
      6. 32.2.5: Development of Fruit and Fruit Types
      7. 32.2.6: Fruit and Seed Dispersal
    3. 32.3: Asexual Reproduction
      1. 32.3.0: Asexual Reproduction in Plants
      2. 32.3.1: Natural and Artificial Methods of Asexual Reproduction in Plants
      3. 32.3.2: Plant Life Spans
  33. 33: The Animal Body: Basic Form and Function
    1. 33.1: Animal Form and Function
      1. 33.1.0: Characteristics of the Animal Body
      2. 33.1.1: Body Plans
      3. 33.1.2: Limits on Animal Size and Shape
      4. 33.1.3: Limiting Effects of Diffusion on Size and Development
      5. 33.1.4: Animal Bioenergetics
      6. 33.1.5: Animal Body Planes and Cavities
    2. 33.2: Animal Primary Tissues
      1. 33.2.0: Epithelial Tissues
      2. 33.2.1: Connective Tissues: Loose, Fibrous, and Cartilage
      3. 33.2.2: Connective Tissues: Bone, Adipose, and Blood
      4. 33.2.3: Muscle Tissues and Nervous Tissues
    3. 33.3: Homeostasis
      1. 33.3.0: Homeostatic Process
      2. 33.3.1: Control of Homeostasis
      3. 33.3.2: Homeostasis: Thermoregulation
      4. 33.3.3: Heat Conservation and Dissipation
  34. 34: Animal Nutrition and the Digestive System
    1. 34.1: Digestive Systems
      1. 34.1.0: Digestive Systems
      2. 34.1.1: Herbivores, Omnivores, and Carnivores
      3. 34.1.2: Invertebrate Digestive Systems
      4. 34.1.3: Vertebrate Digestive Systems
      5. 34.1.4: Digestive System: Mouth and Stomach
      6. 34.1.5: Digestive System: Small and Large Intestines
    2. 34.2: Nutrition and Energy Production
      1. 34.2.0: Food Requirements and Essential Nutrients
      2. 34.2.1: Food Energy and ATP
    3. 34.3: Digestive System Processes
      1. 34.3.0: Ingestion
      2. 34.3.1: Digestion and Absorption
      3. 34.3.2: Elimination
    4. 34.4: Digestive System Regulation
      1. 34.4.0: Neural Responses to Food
      2. 34.4.1: Hormonal Responses to Food
  35. 35: The Nervous System
    1. 35.1: Neurons and Glial Cells
      1. 35.1.0: Neurons and Glial Cells
      2. 35.1.1: Neurons
      3. 35.1.2: Glia
    2. 35.2: How Neurons Communicate
      1. 35.2.0: Nerve Impulse Transmission within a Neuron: Resting Potential
      2. 35.2.1: Nerve Impulse Transmission within a Neuron: Action Potential
      3. 35.2.2: Synaptic Transmission
      4. 35.2.3: Signal Summation
      5. 35.2.4: Synaptic Plasticity
    3. 35.3: The Nervous System
      1. 35.3.0: The Nervous System
    4. 35.4: The Central Nervous System
      1. 35.4.0: Brain: Cerebral Cortex and Brain Lobes
      2. 35.4.1: Brain: Midbrain and Brain Stem
      3. 35.4.2: Spinal Cord
    5. 35.5: The Peripheral Nervous System
      1. 35.5.0: Autonomic Nervous System
      2. 35.5.1: Sensory-Somatic Nervous System
    6. 35.6: Nervous System Disorders
      1. 35.6.0: Neurodegenerative Disorders
      2. 35.6.1: Neurodevelopmental Disorders: Autism and ADHD
      3. 35.6.2: Neurodevelopmental Disorders: Mental Illnesses
      4. 35.6.3: Other Neurological Disorders
  36. 36: Sensory Systems
    1. 36.1: Sensory Processes
      1. 36.1.0: Reception
      2. 36.1.1: Transduction and Perception
    2. 36.2: Somatosensation
      1. 36.2.0: Somatosensory Receptors
      2. 36.2.1: Integration of Signals from Mechanoreceptors
      3. 36.2.2: Thermoreception
    3. 36.3: Taste and Smell
      1. 36.3.0: Tastes and Odors
      2. 36.3.1: Reception and Transduction
    4. 36.4: Hearing and Vestibular Sensation
      1. 36.4.0: Sound
      2. 36.4.1: Reception of Sound
      3. 36.4.2: Transduction of Sound
      4. 36.4.3: The Vestibular System
      5. 36.4.4: Balance and Determining Equilibrium
    5. 36.5: Vision
      1. 36.5.0: Light
      2. 36.5.1: Anatomy of the Eye
      3. 36.5.2: Transduction of Light
      4. 36.5.3: Visual Processing
  37. 37: The Endocrine System
    1. 37.1: Types of Hormones
      1. 37.1.0: Hormone Functions
      2. 37.1.1: Lipid-Derived, Amino Acid-Derived, and Peptide Hormones
    2. 37.2: How Hormones Work
      1. 37.2.0: How Hormones Work
      2. 37.2.1: Intracellular Hormone Receptors
      3. 37.2.2: Plasma Membrane Hormone Receptors
    3. 37.3: Regulation of Body Processes
      1. 37.3.0: Hormonal Regulation of the Excretory System
      2. 37.3.1: Hormonal Regulation of the Reproductive System
      3. 37.3.2: Hormonal Regulation of Metabolism
      4. 37.3.3: Hormonal Control of Blood Calcium Levels
      5. 37.3.4: Hormonal Regulation of Growth
      6. 37.3.5: Hormonal Regulation of Stress
    4. 37.4: Regulation of Hormone Production
      1. 37.4.0: Humoral, Hormonal, and Neural Stimuli
    5. 37.5: Endocrine Glands
      1. 37.5.0: Hypothalamic-Pituitary Axis
      2. 37.5.1: Thyroid Gland
      3. 37.5.2: Parathyroid Glands
      4. 37.5.3: Adrenal Glands
      5. 37.5.4: Pancreas
      6. 37.5.5: Pineal Gland and Gonads
      7. 37.5.6: Organs with Secondary Endocrine Functions
  38. 38: The Musculoskeletal System
    1. 38.1: Types of Skeletal Systems
      1. 38.1.0: Functions of the Musculoskeletal System
      2. 38.1.1: Types of Skeletal Systems
      3. 38.1.2: Human Axial Skeleton
      4. 38.1.3: Human Appendicular Skeleton
    2. 38.2: Bone
      1. 38.2.0: Bone
      2. 38.2.1: Cell Types in Bones
      3. 38.2.2: Bone Development
      4. 38.2.3: Growth of Bone
      5. 38.2.4: Bone Remodeling and Repair
    3. 38.3: Joints and Skeletal Movement
      1. 38.3.0: Classification of Joints on the Basis of Structure and Function
      2. 38.3.1: Movement at Synovial Joints
      3. 38.3.2: Types of Synovial Joints
      4. 38.3.3: Bone and Joint Disorders
    4. 38.4: Muscle Contraction and Locomotion
      1. 38.4.0: Structure and Function of the Muscular System
      2. 38.4.1: Skeletal Muscle Fibers
      3. 38.4.2: Sliding Filament Model of Contraction
      4. 38.4.3: ATP and Muscle Contraction
      5. 38.4.4: Regulatory Proteins
      6. 38.4.5: Excitation–Contraction Coupling
      7. 38.4.6: Control of Muscle Tension
  39. 39: The Respiratory System
    1. 39.1: Systems of Gas Exchange
      1. 39.1.0: The Respiratory System and Direct Diffusion
      2. 39.1.1: Skin, Gills, and Tracheal Systems
      3. 39.1.2: Amphibian and Bird Respiratory Systems
      4. 39.1.3: Mammalian Systems and Protective Mechanisms
    2. 39.2: Gas Exchange across Respiratory Surfaces
      1. 39.2.0: Gas Pressure and Respiration
      2. 39.2.1: Basic Principles of Gas Exchange
      3. 39.2.2: Lung Volumes and Capacities
      4. 39.2.3: Gas Exchange across the Alveoli
    3. 39.3: Breathing
      1. 39.3.0: The Mechanics of Human Breathing
      2. 39.3.1: Types of Breathing
      3. 39.3.2: The Work of Breathing
      4. 39.3.3: Dead Space: V/Q Mismatch
    4. 39.4: Transport of Gases in Human Bodily Fluids
      1. 39.4.0: Transport of Oxygen in the Blood
      2. 39.4.1: Transport of Carbon Dioxide in the Blood
  40. 40: The Circulatory System
    1. 40.1: Overview of the Circulatory System
      1. 40.1.0: The Role of the Circulatory System
      2. 40.1.1: Open and Closed Circulatory Systems
      3. 40.1.2: Types of Circulatory Systems in Animals
    2. 40.2: Components of the Blood
      1. 40.2.0: The Role of Blood in the Body
      2. 40.2.1: Red Blood Cells
      3. 40.2.2: White Blood Cells
      4. 40.2.3: Platelets and Coagulation Factors
      5. 40.2.4: Plasma and Serum
    3. 40.3: Mammalian Heart and Blood Vessels
      1. 40.3.0: Structures of the Heart
      2. 40.3.1: Arteries, Veins, and Capillaries
      3. 40.3.2: The Cardiac Cycle
    4. 40.4: Blood Flow and Blood Pressure Regulation
      1. 40.4.0: Blood Flow Through the Body
      2. 40.4.1: Blood Pressure
  41. 41: Osmotic Regulation and the Excretory System
    1. 41.1: Osmoregulation and Osmotic Balance
      1. 41.1.0: Introduction to Osmoregulation
      2. 41.1.1: Transport of Electrolytes across Cell Membranes
      3. 41.1.2: Concept of Osmolality and Milliequivalent
      4. 41.1.3: Osmoregulators and Osmoconformers
    2. 41.2: Nitrogenous Wastes
      1. 41.2.0: Nitrogenous Waste in Terrestrial Animals: The Urea Cycle
      2. 41.2.1: Nitrogenous Waste in Birds and Reptiles: Uric Acid
    3. 41.3: Excretion Systems
      1. 41.3.0: Contractile Vacuoles in Microorganisms
      2. 41.3.1: Flame Cells of Planaria and Nephridia of Worms
      3. 41.3.2: Malpighian Tubules of Insects
    4. 41.4: Human Osmoregulatory and Excretory Systems
      1. 41.4.0: Kidney Structure
      2. 41.4.1: Nephron: The Functional Unit of the Kidney
      3. 41.4.2: Kidney Function and Physiology
    5. 41.5: Hormonal Control of Osmoregulatory Functions
      1. 41.5.0: Epinephrine and Norepinephrine
      2. 41.5.1: Other Hormonal Controls for Osmoregulation
  42. 42: The Immune System
    1. 42.1: Innate Immune Response
      1. 42.1.0: Innate Immune Response
      2. 42.1.1: Physical and Chemical Barriers
      3. 42.1.2: Pathogen Recognition
      4. 42.1.3: Natural Killer Cells
      5. 42.1.4: The Complement System
    2. 42.2: Adaptive Immune Response
      1. 42.2.0: Antigen-presenting Cells: B and T cells
      2. 42.2.1: Humoral Immune Response
      3. 42.2.2: Cell-Mediated Immunity
      4. 42.2.3: Cytotoxic T Lymphocytes and Mucosal Surfaces
      5. 42.2.4: Immunological Memory
      6. 42.2.5: Regulating Immune Tolerance
    3. 42.3: Antibodies
      1. 42.3.0: Antibody Structure
      2. 42.3.1: Antibody Functions
    4. 42.4: Disruptions in the Immune System
      1. 42.4.0: Immunodeficiency
      2. 42.4.1: Hypersensitivities
  43. 43: Animal Reproduction and Development
    1. 43.1: Reproduction Methods
      1. 43.1.0: Methods of Reproducing
      2. 43.1.1: Types of Sexual and Asexual Reproduction
      3. 43.1.2: Sex Determination
    2. 43.2: Fertilization
      1. 43.2.0: External and Internal Fertilization
      2. 43.2.1: The Evolution of Reproduction
    3. 43.3: Human Reproductive Anatomy and Gametogenesis
      1. 43.3.0: Male Reproductive Anatomy
      2. 43.3.1: Female Reproductive Anatomy
      3. 43.3.2: Gametogenesis (Spermatogenesis and Oogenesis)
    4. 43.4: Hormonal Control of Human Reproduction
      1. 43.4.0: Male Hormones
      2. 43.4.1: Female Hormones
    5. 43.5: Fertilization and Early Embryonic Development
      1. 43.5.0: Fertilization
      2. 43.5.1: Cleavage, the Blastula Stage, and Gastrulation
    6. 43.6: Organogenesis and Vertebrate Formation
      1. 43.6.0: Organogenesis
      2. 43.6.1: Vertebrate Axis Formation
    7. 43.7: Human Pregnancy and Birth
      1. 43.7.0: Human Gestation
      2. 43.7.1: Labor and Birth
      3. 43.7.2: Contraception and Birth Control
      4. 43.7.3: Infertility
  44. 44: Ecology and the Biosphere
    1. 44.1: The Scope of Ecology
      1. 44.1.0: Introduction to Ecology
      2. 44.1.1: Organismal Ecology and Population Ecology
      3. 44.1.2: Community Ecology and Ecosystem Ecology
    2. 44.2: Biogeography
      1. 44.2.0: Biogeography
      2. 44.2.1: Energy Sources
      3. 44.2.2: Temperature and Water
      4. 44.2.3: Inorganic Nutrients and Other Factors
      5. 44.2.4: Abiotic Factors Influencing Plant Growth
    3. 44.3: Terrestrial Biomes
      1. 44.3.0: What constitutes a biome?
      2. 44.3.1: Tropical Wet Forest and Savannas
      3. 44.3.2: Subtropical Deserts and Chaparral
      4. 44.3.3: Temperate Grasslands
      5. 44.3.4: Temperate Forests
      6. 44.3.5: Boreal Forests and Arctic Tundra
    4. 44.4: Aquatic Biomes
      1. 44.4.0: Abiotic Factors Influencing Aquatic Biomes
      2. 44.4.1: Marine Biomes
      3. 44.4.2: Estuaries: Where the Ocean Meets Fresh Water
      4. 44.4.3: Freshwater Biomes
    5. 44.5: Climate and the Effects of Global Climate Change
      1. 44.5.0: Climate and Weather
      2. 44.5.1: Causes of Global Climate Change
      3. 44.5.2: Evidence of Global Climate Change
      4. 44.5.3: Past and Present Effects of Climate Change
  45. 45: Population and Community Ecology
    1. 45.1: Population Demography
      1. 45.1.0: Population Demography
      2. 45.1.1: Population Size and Density
      3. 45.1.2: Species Distribution
      4. 45.1.3: The Study of Population Dynamics
    2. 45.2: Environmental Limits to Population Growth
      1. 45.2.0: Exponential Population Growth
      2. 45.2.1: Logistic Population Growth
      3. 45.2.2: Density-Dependent and Density-Independent Population Regulation
    3. 45.3: Life History Patterns
      1. 45.3.0: Life History Patterns and Energy Budgets
      2. 45.3.1: Theories of Life History
    4. 45.4: Human Population Growth
      1. 45.4.0: Human Population Growth
      2. 45.4.1: Overcoming Density-Dependent Regulation
      3. 45.4.2: Age Structure, Population Growth, and Economic Development
    5. 45.5: Community Ecology
      1. 45.5.0: The Role of Species within Communities
      2. 45.5.1: Predation, Herbivory, and the Competitive Exclusion Principle
      3. 45.5.2: Symbiosis
      4. 45.5.3: Ecological Succession
    6. 45.6: Innate Animal Behavior
      1. 45.6.0: Introduction to Animal Behavior
      2. 45.6.1: Movement and Migration
      3. 45.6.2: Animal Communication and Living in Groups
      4. 45.6.3: Altruism and Populations
      5. 45.6.4: Mating Systems and Sexual Selection
    7. 45.7: Learned Animal Behavior
      1. 45.7.0: Simple Learned Behaviors
      2. 45.7.1: Conditioned Behavior
      3. 45.7.2: Cognitive Learning and Sociobiology
  46. 46: Ecosystems
    1. 46.1: Ecology of Ecosystems
      1. 46.1.0: Ecosystem Dynamics
      2. 46.1.1: Food Chains and Food Webs
      3. 46.1.2: Studying Ecosystem Dynamics
      4. 46.1.3: Modeling Ecosystem Dynamics
    2. 46.2: Energy Flow through Ecosystems
      1. 46.2.0: Strategies for Acquiring Energy
      2. 46.2.1: Productivity within Trophic Levels
      3. 46.2.2: Transfer of Energy between Trophic Levels
      4. 46.2.3: Ecological Pyramids
      5. 46.2.4: Biological Magnification
    3. 46.3: Biogeochemical Cycles
      1. 46.3.0: Biogeochemical Cycles
      2. 46.3.1: The Water (Hydrologic) Cycle
      3. 46.3.2: The Carbon Cycle
      4. 46.3.3: The Nitrogen Cycle
      5. 46.3.4: The Phosphorus Cycle
      6. 46.3.5: The Sulfur Cycle
  47. 47: Conservation Biology and Biodiversity
    1. 47.1: The Biodiversity Crisis
      1. 47.1.0: Loss of Biodiversity
      2. 47.1.1: Types of Biodiversity
      3. 47.1.2: Biodiversity Change through Geological Time
      4. 47.1.3: The Pleistocene Extinction
      5. 47.1.4: Present-Time Extinctions
    2. 47.2: The Importance of Biodiversity to Human Life
      1. 47.2.0: Human Health and Biodiversity
      2. 47.2.1: Agricultural Diversity
      3. 47.2.2: Managing Fisheries
    3. 47.3: Threats to Biodiversity
      1. 47.3.0: Habitat Loss and Sustainability
      2. 47.3.1: Overharvesting
      3. 47.3.2: Exotic Species
      4. 47.3.3: Climate Change and Biodiversity
    4. 47.4: Preserving Biodiversity
      1. 47.4.0: Measuring Biodiversity
      2. 47.4.1: Changing Human Behavior in Response to Biodiversity Loss
      3. 47.4.2: Ecological Restoration

37.3: Regulation of Body Processes

37.3.1: Hormonal Regulation of the Excretory System

The contrasting actions of antidiruetic hormone and aldosterone work to regulate the level of water in the body.

Learning Objective

Explain how the actions of different hormones regulate the excretory system

Key Points

  • The hypothalamus monitors the amount of water in the body by sensing the concentration of electrolytes in the blood; a high concentration of electrolytes means that the level of water in the body is low.
  • Antidiuretic hormone (ADH), produced by the hypothalamus and released by the posterior pituitary, causes more water to be retained by the kidneys when water levels in the body are low.
  • ADH effects water retention by creating special channels for water, called aquaporins, inside the kidneys so that more water can be reabsorbed before it is excreted.
  • Aldosterone, produced by the adrenal cortex, causes the retention of water in the body by increasing the levels of sodium and potassium ions in the blood, which causes the body to reabsorb more water.
  • When blood pressure is low, the enzyme renin is released, which cleaves the protein angiotensinogen into angiotensin I, which is further converted into angiotensin II.
  • Angiotensin II signals the adrenal cortex to release aldosterone, which then increases the retention of sodium ions, enhancing the secretion of postassium ions, resulting in water retention and an increase in blood pressure.

Key Terms

aldosterone

a mineralocorticoid hormone, secreted by the adrenal cortex, that regulates the balance of sodium and potassium in the body

aquaporin

any of a class of proteins that form pores in the membrane of biological cells

electrolyte

any of the various ions (such as sodium or chloride) that regulate the electric charge on cells and the flow of water across their membranes

mineralocorticoid

any of a group of steroid hormones, characterised by their similarity to aldosterone and their influence on salt and water metabolism

renin

a circulating enzyme released by mammalian kidneys that converts angiotensinogen to angiotensin-I that plays a role in maintaining blood pressure

osmoreceptor

a sensory receptor primarily found in the hypothalamus of most homeothermic organisms that detects changes in osmotic pressure

antidiuretic hormone

a hormone secreted by the posterior pituitary gland that regulates the amount of water excreted by the kidneys

Hormonal Regulation of the Excretory System

Maintaining a proper water balance in the body is important to avoid dehydration or over-hydration (hyponatremia). The water concentration of the body is monitored by osmoreceptors in the hypothalamus, which detect the concentration of electrolytes in the extracellular fluid. The concentration of electrolytes in the blood rises when there is water loss caused by excessive perspiration, inadequate water intake, or low blood volume due to blood loss. An increase in blood electrolyte levels results in a neuronal signal being sent from the osmoreceptors in hypothalamic nuclei. The anterior pituitary is composed of glandular cells that secrete protein hormones. The pituitary gland has two components: anterior and posterior. The posterior pituitary is an extension of the hypothalamus. It is composed largely of neurons that are continuous with the hypothalamus.

Antidiuretic Hormone (ADH)

The hypothalamus produces a polypeptide hormone known as antidiuretic hormone (ADH), which is transported to and released from the posterior pituitary gland. The principal action of ADH is to regulate the amount of water excreted by the kidneys. As ADH (which is also known as vasopressin) causes direct water reabsorption from the kidney tubules, salts and wastes are concentrated in what will eventually be excreted as urine. The hypothalamus controls the mechanisms of ADH secretion, either by regulating blood volume or the concentration of water in the blood. Dehydration or physiological stress can cause an increase of osmolarity above threshold levels, which, in turn, raises ADH secretion and water retention, causing an increase in blood pressure. ADH travels in the bloodstream to the kidneys where it changes the kidneys to become more permeable to water by temporarily inserting water channels, aquaporins, into the kidney tubules. Water moves out of the kidney tubules through the aquaporins, reducing urine volume. The water is reabsorbed into the capillaries, lowering blood osmolarity back toward normal. As blood osmolarity decreases, a negative feedback mechanism reduces osmoreceptor activity in the hypothalamus; ADH secretion is reduced. ADH release can be reduced by certain substances, including alcohol, which can cause increased urine production and dehydration.

Chronic underproduction of ADH or a mutation in the ADH receptor results in diabetes insipidus. If the posterior pituitary does not release enough ADH, water cannot be retained by the kidneys and is lost as urine. This causes increased thirst, but water taken in is lost again and must be continually consumed. If the condition is not severe, dehydration may not occur, but severe cases can lead to electrolyte imbalances due to dehydration.

Another hormone responsible for maintaining electrolyte concentrations in extracellular fluids is aldosterone, a steroid hormone that is produced by the adrenal cortex. In contrast to ADH, which promotes the reabsorption of water to maintain proper water balance, aldosterone maintains proper water balance by enhancing Na+ reabsorption and K+ secretion from extracellular fluid of the cells in kidney tubules. Because it is produced in the cortex of the adrenal gland and affects the concentrations of minerals Na+ and K+, aldosterone is referred to as a mineralocorticoid, a corticosteroid that affects ion and water balance. Aldosterone release is stimulated by a decrease in blood sodium levels, blood volume, or blood pressure, or an increase in blood potassium levels. It also prevents the loss of Na+ from sweat, saliva, and gastric juice. The reabsorption of Na+ also results in the osmotic reabsorption of water, which alters blood volume and blood pressure.

Aldosterone production can be stimulated by low blood pressure, which triggers a sequence of chemical release . When blood pressure drops, the renin-angiotensin-aldosterone system (RAAS) is activated. Cells in the juxtaglomerular apparatus, which regulates the functions of the nephrons of the kidney, detect this and release renin. Renin, an enzyme, circulates in the blood, reacting with a plasma protein produced by the liver called angiotensinogen. When angiotensinogen is cleaved by renin, it produces angiotensin I, which is then converted into angiotensin II in the lungs. Angiotensin II functions as a hormone, causing the release of the hormone aldosterone by the adrenal cortex, resulting in increased Na+ reabsorption, water retention, and an increase in blood pressure. Angiotensin II, in addition to being a potent vasoconstrictor, also causes an increase in ADH and increased thirst, both of which help to raise blood pressure.

Action of aldosterone

Action of aldosterone

ADH and aldosterone increase blood pressure and volume. Angiotensin II stimulates release of these hormones. Angiotensin II, in turn, is formed when renin cleaves angiotensin. This increases water retention and blood pressure.

37.3.2: Hormonal Regulation of the Reproductive System

Male and female gonads are regulated by FSH and LH from the pituitary; their production is stimulated by GnRH, secreted by the hypothalamus.

Learning Objective

Explain the regulation of the male and female reproductive systems

Key Points

  • In males, FSH stimulates the production of sperm cells by signaling them to undergo meiosis, while in females, FSH stimulates the growth of the ovum inside the follicle of the ovary.
  • In males, LH stimulates the Leydig cells within the testes to produce testosterone, which encourages sperm production and leads to secondary sexual characteristics.
  • In females, LH plays a crucial role in signaling ovulation, as well as stimulating the production of other hormones that will prepare the body for pregnancy.
  • Other hormones involved in the female reproductive system are oxytocin, which signals the uterus to contract during childbirth, and prolactin, which stimulates milk production.

Key Terms

prolactin

a peptide gonadotrophic hormone secreted by the pituitary gland; it stimulates growth of the mammary glands and lactation in females

inhibin

a peptide hormone, secreted by the gonads, which inhibits the secretion of follicle-stimulating hormone

gonad

a sex organ that produces gametes; specifically, a testicle or ovary

luteinizing hormone

a hormone, produced by part of the pituitary gland, that stimulates ovulation and the development of the corpus luteum in female mammals, and the production of androgens by male mammals

follicle stimulating hormone

a gonadotropic glycoprotein hormone, secreted in the anterior pituitary, that stimulates the growth of ovarian follicles in female mammals, and induces spermatogenesis in male mammals

gonadotropin-releasing hormone

a trophicpeptide responsible for the release of follicle stimulating hormone and lutenizing hormone from the anterior pituitary, synthesized and released from the hypothalamus

androgen

the generic term for any natural or synthetic compound, usually a steroid hormone, that stimulates or controls the development and maintenance of masculine characteristics in vertebrates

Hormonal Regulation of the Reproductive System

Regulation of the reproductive system is a process that requires the action of hormones from the pituitary gland, the adrenal cortex, and the gonads. During puberty, in both males and females, the hypothalamus produces gonadotropin-releasing hormone (GnRH), which stimulates the production and release of follicle stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary gland. These hormones regulate the gonads (testes in males and ovaries in females); they are called gonadotropins. In both males and females, FSH stimulates gamete production and LH stimulates production of hormones by the gonads. An increase in gonad hormone levels inhibits GnRH production through a negative feedback loop .

The negative feedback loop of the male reproductive system

The negative feedback loop of the male reproductive system

GnRH, secreted by the hypothalamus, stimulates the production of FSH and LH from the pituitary gland. These hormones encourage the development of sperm cells within the testicles, which then produce inhibin and inhibit the production of GnRH, FSH and LH in a negative feedback loop.

Regulation of the Male Reproductive System

At the pituitary, GnRH stimulates the synthesis and secretion of the gonadotropins, FSH and LH. These processes are controlled by the size and frequency of GnRH pulses, as well as by feedback from androgens and estrogens. Low-frequency GnRH pulses lead to FSH release, whereas high-frequency GnRH pulses stimulate LH release. In males, FSH stimulates primary spermatocytes to undergo the first division of meiosis, to form secondary spermatocytes, leading to the maturation of sperm cells. FSH also enhances the production of androgen-binding protein by the Sertoli cells of the testes by binding to FSH receptors on their basolateral membranes. FSH production is inhibited by the hormone inhibin, which is released by the testes.

LH stimulates production of the sex hormones (androgens) by the Leydig cells of the testes. It is also called interstitial-cell-stimulating hormone. The most widely-known androgen in males is testosterone, which promotes the production of sperm and masculine characteristics. The adrenal cortex also produces small amounts of testosterone precursor, although the role of this additional hormone production is not fully understood.

Regulation of the Female Reproductive System

In females, FSH stimulates development of egg cells (or ova) in structures called follicles. Follicle cells produce the hormone inhibin, which inhibits FSH production in the female reproductive system. LH also plays a role in the development of ova, induction of ovulation, and stimulation of estradiol and progesterone production by the ovaries . Estradiol and progesterone are steroid hormones that prepare the body for pregnancy. Estradiol produces secondary sex characteristics in females, while both estradiol and progesterone regulate the menstrual cycle.

Regulation of the female reproductive system

Regulation of the female reproductive system

Hormonal regulation of the female reproductive system involves hormones from the hypothalamus, pituitary, and ovaries. GnRH secreted by the hypothalamus stimulates the release of FSH, which stimulates the growth of egg cells, and LH, which signals for the the ovulation of an egg from its follicle. The ovaries, in turn, secrete hormones that play a role in female sexual characteristics.

In addition to producing FSH and LH, the anterior portion of the pituitary gland also produces the hormone prolactin (PRL) in females. Prolactin stimulates the production of milk by the mammary glands, following childbirth. Prolactin levels are regulated by the hypothalamic hormones, prolactin-releasing hormone (PRH) and prolactin-inhibiting hormone (PIH) (which is now known to be dopamine). PRH stimulates the release of prolactin, while PIH inhibits it.

The posterior pituitary releases the hormone oxytocin, which stimulates uterine contractions during childbirth. The uterine smooth muscles are not very sensitive to oxytocin until late in pregnancy, when the number of oxytocin receptors in the uterus peaks. Stretching of tissues in the uterus and cervix stimulates oxytocin release during childbirth. Contractions increase in intensity as blood levels of oxytocin rise via a positive feedback mechanism until the birth is complete. Oxytocin also stimulates the contraction of myoepithelial cells around the milk-producing mammary glands. As these cells contract, milk is forced from the secretory alveoli into milk ducts and is ejected from the breasts in a milk ejection ("let-down") reflex. Oxytocin release is stimulated by the suckling of an infant, which triggers the synthesis of oxytocin in the hypothalamus and its release into circulation at the posterior pituitary.

37.3.3: Hormonal Regulation of Metabolism

The levels of glucose in the blood are regulated by the hormones insulin and glucagon from the pancreas, and T3 and T4 from the thyroid.

Learning Objective

Explain how the hormones glucagon and insulin regulate blood glucose

Key Points

  • When blood glucose levels rise, insulin is secreted by the pancreas, lowering blood glucose by increasing its uptake in cells and stimulating the liver to convert glucose to glycogen, in which form it can be stored.
  • If insulin secretion is impaired, it can result in diabetes mellitus: a disease in which blood glucose levels remain high, leading to excess glucose in the urine, increased urine output, and dehydration, among other symptoms.
  • When blood glucose levels fall, glucagon is secreted by the pancreas, which increases blood glucose levels by stimulating the breakdown of glycogen into glucose and the creation of glucose from amino acids.
  • The basal metabolic rate of the body is controlled by the hormones T3 and T4, produced by the thyroid gland in response to the thyroid stimulating hormone (TSH), produced by the anterior pituitary.
  • T3 and T4 bind to receptors on the mitochondria, causing an increase in the production of ATP, as well as increase in the transcription of genes that help utilize glucose and produce ATP, resulting in higher metabolism of the cell.

Key Terms

hyperthyroidism

the excessive production of hormones by the thyroid

hypothyroidism

the disease state caused by insufficient production of thyroid hormone by the thyroid gland

triiodothyronine

the most powerful thyroid hormone, affecting almost every process in the body, including body temperature, growth, and heart rate

thyroxine

a hormone (an iodine derivative of tyrosine), produced by the thyroid gland, that regulates cell metabolism and growth

gluconeogenesis

the metabolic process in which glucose is formed, mostly in the liver, from non-carbohydrate precursors

glycogenolysis

the production of glucose-1-phosphate by splitting a glucose monomer from glycogen using inorganic phosphate

hypoglycemia

a condition in which blood glucose levels are too low

glycogen

a polysaccharide that is the main form of carbohydrate storage in animals; converted to glucose as needed

glucagon

a hormone, produced by the pancreas, that opposes the action of insulin by stimulating the production of sugar

insulin

a polypeptide hormone that regulates carbohydrate metabolism

Hormonal Regulation of Metabolism

Blood glucose levels vary widely over the course of a day as periods of food consumption alternate with periods of fasting. Insulin and glucagon are the two hormones primarily responsible for maintaining homeostasis of blood glucose levels. Additional regulation is mediated by the thyroid hormones.

Regulation of Blood Glucose Levels: Insulin and Glucagon

Cells of the body require nutrients in order to function. These nutrients are obtained through feeding. In order to manage nutrient intake, storing excess intake, and utilizing reserves when necessary, the body uses hormones to moderate energy stores. Insulin is produced by the beta cells of the pancreas, which are stimulated to release insulin as blood glucose levels rise (for example, after a meal is consumed). Insulin lowers blood glucose levels by enhancing the rate of glucose uptake and utilization by target cells, which use glucose for ATP production. It also stimulates the liver to convert glucose to glycogen, which is then stored by cells for later use. As insulin binds to its target cell via insulin receptors and signal transduction, it triggers the cell to incorporate glucose transport proteins into its membrane. This allows glucose to enter the cell, where it can be used as an energy source. These actions mediated by insulin cause blood glucose concentrations to fall, called a hypoglycemic, or "low sugar" effect, which inhibits further insulin release from beta cells through a negative feedback loop.

Impaired insulin function can lead to a condition called diabetes mellitus, which has many effects on the body . It can be caused by low levels of insulin production by the beta cells of the pancreas, or by reduced sensitivity of tissue cells to insulin. This prevents glucose from being absorbed by cells, causing high levels of blood glucose, or hyperglycemia (high sugar). High blood glucose levels make it difficult for the kidneys to recover all the glucose from nascent urine, resulting in glucose being lost in urine. High glucose levels also result in less water being reabsorbed by the kidneys, causing high amounts of urine to be produced; this may result in dehydration. Over time, high blood glucose levels can cause nerve damage to the eyes and peripheral body tissues, as well as damage to the kidneys and cardiovascular system. Oversecretion of insulin can cause hypoglycemia, low blood glucose levels. This causes insufficient glucose availability to cells, often leading to muscle weakness. It can sometimes cause unconsciousness or death if left untreated.

Diabetes mellitus

Diabetes mellitus

Diabetes mellitus can cause a wide range of symptoms, including nausea, vomiting, blurred vision, lethargy, a frequency in urination, and high levels of glucose in the urine.

When blood glucose levels decline below normal levels, for example between meals or when glucose is utilized during exercise, the hormone glucagon is released from the pancreas. Glucagon raises blood glucose levels, eliciting what is called a hyperglycemic effect, by stimulating the breakdown of glycogen to glucose in skeletal muscle cells and liver cells in a process called glycogenolysis. Glucose can then be utilized as energy by muscle cells and released into circulation by the liver cells. Glucagon also stimulates absorption of amino acids from the blood by the liver, which then converts them to glucose. This process of glucose synthesis is called gluconeogenesis. Rising blood glucose levels inhibit further glucagon release by the pancreas via a negative feedback mechanism. In this way, insulin and glucagon work together to maintain homeostatic glucose levels .

The regulation of blood glucose levels by insulin and glucagon

The regulation of blood glucose levels by insulin and glucagon

As the levels of glucose in the blood rise, insulin stimulates the cells to take up more glucose and signals the liver to convert the excess glucose to glycogen, a form in which it can be stored for later use. When the levels of glucose in the blood fall, glucagon responds by stimulating the breakdown of glycogen into glucose and signals the production of additional glucose from amino acids.

Regulation of Blood Glucose Levels: Thyroid Hormones

The basal metabolic rate, which is the amount of calories required by the body at rest, is determined by two hormones produced by the thyroid gland: thyroxine, also known as tetraiodothyronine or T4, and triiodothyronine, also known as T3. T3 and T4 release from the thyroid gland are stimulated by thyroid-stimulating hormone (TSH), which is produced by the anterior pituitary. These hormones affect nearly every cell in the body except for the adult brain, uterus, testes, blood cells, and spleen. They are transported across the plasma membrane of target cells where they bind to receptors on the mitochondria, resulting in increased ATP production. In the nucleus, T3and T4activate genes involved in energy production and glucose oxidation. This results in increased rates of metabolism and body heat production. This is known as the hormone's calorigenic effect.

Disorders can arise from both the underproduction and overproduction of thyroid hormones. Hypothyroidism, underproduction of the thyroid hormones, can cause a low metabolic rate leading to weight gain, sensitivity to cold, and reduced mental activity, among other symptoms. In children, hypothyroidism can cause cretinism, which can lead to mental retardation and growth defects. Hyperthyroidism, the overproduction of thyroid hormones, can lead to an increased metabolic rate, which may cause weight loss, excess heat production, sweating, and an increased heart rate.

37.3.4: Hormonal Control of Blood Calcium Levels

Blood levels of calcium are regulated by the parathyroid hormone, which acts on the bones, kidneys, and intestines to keep levels constant.

Learning Objective

Explain how blood calcium levels are regulated by parathyroid hormone

Key Points

  • The parathyroid hormone (PTH), secreted by the parathyroid glands, is responsible for regulating blood calcium levels; it is released whenever blood calcium levels are low.
  • PTH increases blood calcium levels by stimulating osteoclasts, which break down bone to release calcium into the blood stream.
  • PTH increases blood calcium levels by increasing the amount of calcium resorbed by the kidneys before it can be excreted in the urine.
  • PTH increases blood calcium levels by triggering the formation of calcitriol, which increases absorption of dietary calcium through the intestines.
  • Calcitonin, a hormone produced by the thyroid, acts in opposition to PTH by inhibiting osteoclasts, stimulating osteoblasts, and increasing excretion of calcium into the urine by the kidneys.

Key Terms

osteoclast

a large multinuclear cell associated with the resorption of bone

calcitriol

the active metabolite 1,25-dihydroxycholecalciferol of vitamin D3 that is involved in the absorption of calcium

hyperparathyroidism

an abnormal increase in parathyroid gland activity

hypoparathyroidism

deficiency of parathyroid hormone

calcitonin

a hormone, secreted by parenchymal cells, that regulates calcium and phosphate metabolism

osteoblast

a mononucleate cell from which bone develops

parathyroid hormone

a polypeptide hormone that is released by the chief cells of the parathyroid glands and is involved in raising the levels of calcium ions in the blood

Hormonal Control of Blood Calcium Levels

Regulation of blood calcium concentrations is important for generation of muscle contractions and nerve impulses, which are electrically stimulated. If calcium levels get too high, membrane permeability to sodium decreases and membranes become less responsive. If calcium levels get too low, membrane permeability to sodium increases and convulsions or muscle spasms may result.

Blood calcium levels are regulated by parathyroid hormone (PTH), which is produced by the parathyroid glands. PTH is released in response to low blood calcium levels. It increases calcium levels by targeting the skeleton, the kidneys, and the intestine . In the skeleton, PTH stimulates osteoclasts, which are cells that cause bone to be reabsorbed, releasing calcium from bone into the blood. PTH also inhibits osteoblasts, cells which deposit bone, reducing calcium deposition in bone. In the intestines, PTH increases dietary calcium absorption and in the kidneys, PTH stimulates re-absorption of the calcium. While PTH acts directly on the kidneys to increase calcium re-absorption, its effects on the intestine are indirect. PTH triggers the formation of calcitriol, an active form of vitamin D, which acts on the intestines to increase absorption of dietary calcium. PTH release is inhibited by rising blood calcium levels.

Regulation of blood calcium levels

Regulation of blood calcium levels

Parathyroid hormone (PTH) is released in response to low blood calcium levels. It increases blood calcium levels by stimulating the resorption of bones, increasing calcium resorption in the kidneys, and indirectly increasing calcium absorption in the intestines.

Hyperparathyroidism results from an overproduction of PTH, which leads to excessive amounts of calcium being removed from bones and introduced into blood circulation. This may produce structural weakness of the bones, which can lead to deformation and fractures, plus nervous system impairment due to high blood calcium levels. Hypoparathyroidism, the underproduction of PTH, results in extremely low levels of blood calcium, which causes impaired muscle function and may result in tetany (severe sustained muscle contraction).

The hormone calcitonin, which is produced by the parafollicular (or C) cells of the thyroid, has the opposite effect on blood calcium levels as PTH. Calcitonin decreases blood calcium levels by inhibiting osteoclasts, stimulating osteoblasts, and stimulating calcium excretion by the kidneys. This results in calcium being added to the bones to promote structural integrity. Calcitonin is most important in children (when it stimulates bone growth), during pregnancy (when it reduces maternal bone loss), and during prolonged starvation (because it reduces bone mass loss). In healthy, nonpregnant, unstarved adults, the role of calcitonin is unclear.

37.3.5: Hormonal Regulation of Growth

Body growth is controlled by growth hormone (GH), produced by the anterior pituitary, and IGF-1, whose production is stimulated by GH.

Learning Objective

Describe the hormonal regulation of growth

Key Points

  • Growth hormone binds to receptors on target cells, causing mature cartilage cells to divide, creating new cartilage tissue.
  • Growth hormone stimulates the production of IGF-1, a hormone that increases the uptake of amino acids when they are at high levels in the blood, so that they can be formed into new proteins.
  • Growth hormone-releasing hormone stimulates the production of GH by the anterior pituitary, while growth hormone-inhibiting hormone inhibits its production.
  • When growth hormone production is abnormally low in children, it can result in pituitary dwarfism, in which individuals can be less than 30 inches tall; when growth hormone production is high in children, it can result in gigantism, in which individuals can be over 8 feet tall.

Key Terms

gigantism

a condition caused by an over-production of growth hormone, resulting in excessive bone growth

somatostatin

a polypeptide hormone, secreted by the pancreas, that inhibits the production of certain other hormones

growth hormone

any polypeptide hormone secreted by the pituitary gland that promotes growth and regulates the metabolism of carbohydrates, proteins, and lipids

Hormonal Regulation of Growth

Hormonal regulation is required for the growth and replication of most cells in the body. Growth hormone (GH), produced by the anterior portion of the pituitary gland, accelerates the rate of protein synthesis, particularly in skeletal muscle and bones. Effects of growth hormone on the tissues of the body can generally be described as anabolic (building up). Like most other protein hormones, GH acts by interacting with a specific receptor on the surface of cells. Increased height during childhood is the most widely-known effect of GH. Height appears to be stimulated by at least two mechanisms: Because polypeptide hormones are not fat-soluble, they cannot penetrate cell membranes. Thus, GH exerts some of its effects by binding to receptors on target cells, where it activates a pathway that directly stimulates division and multiplication of chondrocytes of cartilage.

GH also stimulates, through another pathway, the production of insulin-like growth factor 1 (IGF-1), a hormone homologous to proinsulin. The liver, a major target organ of GH for this process, is the principal site of IGF-1 production. IGF-1 has growth-stimulating effects on a wide variety of tissues. IGFs stimulate the uptake of amino acids from the blood, allowing the formation of new proteins, particularly in skeletal muscle cells, cartilage cells, and other target cells . This is especially important after a meal, when glucose and amino acid concentration levels are high in the blood. GH levels are regulated by two hormones produced by the hypothalamus. GH release is stimulated by growth hormone-releasing hormone (GHRH) and is inhibited by growth hormone-inhibiting hormone (GHIH), also called somatostatin. IGF-1 also has stimulatory effects on osteoblast and chondrocyte activity to promote bone growth.

Effects of growth hormone

Effects of growth hormone

Growth hormone directly accelerates the rate of protein synthesis in skeletal muscle and bones. Insulin-like growth factor 1 (IGF-1) is activated by growth hormone and also allows formation of new proteins in muscle cells and bone.

A balanced production of growth hormone is critical for proper development. Underproduction of GH in adults does not appear to cause any abnormalities, but in children it can result in pituitary dwarfism, in which growth is reduced. Pituitary dwarfism is characterized by symmetric body formation. In some cases, individuals are under 30 inches in height. Oversecretion of growth hormone can lead to gigantism in children, causing excessive growth. In some documented cases, individuals can reach heights of over eight feet. In adults, excessive GH can lead to acromegaly, a condition in which there is enlargement of bones in the face, hands, and feet that are still capable of growth.

37.3.6: Hormonal Regulation of Stress

The adrenal glands respond to either short-term or long-term stressors by releasing different hormones that act differently on the body.

Learning Objective

Describe the role of the adrenal glands in the "fight-or-flight" response and the body's reaction to stress

Key Points

  • When the body senses stress, the hypothalamus signals the adrenal medulla to release epinephrine or norepinephrine, or the anterior pituitary to release ACTH.
  • In short-term stressful situations, such as when a threat is perceived, epinephrine (adrenaline) and norepinephrine (noradrenaline) are released to prepare the body for a "fight-or-flight" response.
  • Epinephrine and norepinephrine act to provide a burst of energy to the body by stimulating the breakdown of glycogen into glucose, increasing the heart rate, and dilating the bronchioles.
  • In long-term stress situations, such as when the body must deal with injury or illness, ACTH is released, stimulating the production of corticosteroids, which include glucocorticoids and mineralocorticoids.
  • Glucocorticoids stimulate the synthesis of glucose and inhibit the immune system.
  • Mineralocorticoids regulate ion and water balance of the body by stimulating the kidneys to excrete less water and sodium ions in the urine.

Key Terms

mineralocorticoid

any of a group of steroid hormones, characterised by their similarity to aldosterone and their influence on salt and water metabolism

corticosteroid

any of a group of steroid hormones, secreted by the adrenal cortex, that are involved in a large range of physiological systems

norepinephrine

a neurotransmitter found in the locus coeruleus which is synthesized from dopamine

epinephrine

(adrenaline) an amino acid-derived hormone secreted by the adrenal gland in response to stress

catecholamine

any of a class of aromatic amines derived from pyrocatechol that are hormones produced by the adrenal gland

glucocorticoid

any of a group of steroid hormones, produced by the adrenal cortex, that are involved in metabolism and have anti-inflammatory properties

adrenocorticotropic hormone

a peptide hormone, secreted by the pituitary gland, that stimulates the secretion of other hormones

Hormonal Regulation of Stress

When a threat or danger is perceived, the body responds by releasing hormones that will ready it for the "fight-or-flight" response. The effects of this response are familiar to anyone who has been in a stressful situation: increased heart rate, dry mouth, and hair standing erect.

The sympathetic nervous system regulates the stress response via the hypothalamus. Stressful stimuli cause the hypothalamus to signal the adrenal medulla (which mediates short-term stress responses) via nerve impulses, and the adrenal cortex, which mediates long-term stress responses via the hormone adrenocorticotropic hormone (ACTH), which is produced by the anterior pituitary.

Short-term Stress Response

Interactions of the endocrine hormones have evolved to ensure the body's internal environment remains stable. Stressors are stimuli that disrupt homeostasis. The sympathetic division of the vertebrate autonomic nervous system has evolved the fight-or-flight response to counter stress-induced disruptions of homeostasis. In the initial alarm phase, the sympathetic nervous system stimulates an increase in energy levels through increased blood glucose levels. This prepares the body for physical activity that may be required to respond to stress: to either fight for survival or to flee from danger .

Fight-or-flight response

Fight-or-flight response

When an animal feels threatened, epinephrine and norepinephrine released by the adrenal medulla prepare the body to fight a threat or flee from it by breaking down stores of glycogen, which provides an immediate boost of energy.

When presented with a stressful situation, the body responds by calling for the release of hormones that provide a burst of energy. The hormones epinephrine (also known as adrenaline) and norepinephrine (also known as noradrenaline) are released by the adrenal medulla. Epinephrine and norepinephrine increase blood glucose levels by stimulating the liver and skeletal muscles to break down glycogen and by stimulating glucose release by liver cells. Additionally, these hormones increase oxygen availability to cells by increasing the heart rate and dilating the bronchioles. The hormones also prioritize body function by increasing blood supply to essential organs, such as the heart, brain, and skeletal muscles, while restricting blood flow to organs not in immediate need, such as the skin, digestive system, and kidneys. Epinephrine and norepinephrine are collectively called catecholamines.

Long-term Stress Response

Some stresses, such as illness or injury, can last for a long time. Glycogen reserves, which provide energy in the short-term response to stress, are exhausted after several hours and cannot meet long-term energy needs. If glycogen reserves were the only energy source available, neural functioning could not be maintained once the reserves became depleted due to the nervous system's high requirement for glucose. In this situation, the body has evolved a response to counter long-term stress through the actions of the glucocorticoids, which ensure that long-term energy requirements can be met. The glucocorticoids mobilize lipid and protein reserves, stimulate gluconeogenesis, conserve glucose for use by neural tissue, and stimulate the conservation of salts and water.

Long-term stress response differs from short-term stress response. The body cannot sustain the bursts of energy mediated by epinephrine and norepinephrine for long times. Instead, other hormones come into play. In a long-term stress response, the hypothalamus triggers the release of ACTH from the anterior pituitary gland. The adrenal cortex is stimulated by ACTH to release steroid hormones called corticosteroids. Corticosteroids turn on transcription of certain genes in the nuclei of target cells. They change enzyme concentrations in the cytoplasm and affect cellular metabolism.

There are two main corticosteroids: glucocorticoids, such as cortisol, and mineralocorticoids, such as aldosterone. These hormones target the breakdown of fat into fatty acids in the adipose tissue. The fatty acids are released into the bloodstream for other tissues to use for ATP production. The glucocorticoids primarily affect glucose metabolism by stimulating glucose synthesis. Glucocorticoids also have anti-inflammatory properties through inhibition of the immune system. For example, cortisone is used as an anti-inflammatory medication; however, it cannot be used long term as it increases susceptibility to disease due to its immune-suppressing effects. Mineralocorticoids function to regulate ion and water balance of the body. The hormone aldosterone stimulates the reabsorption of water and sodium ions in the kidney, which results in increased blood pressure and volume.

Hypersecretion of glucocorticoids can cause a condition known as Cushing's disease, characterized by a shifting of fat storage areas of the body. This can cause the accumulation of adipose tissue in the face and neck, and excessive glucose in the blood. Hyposecretion of the corticosteroids can cause Addison's disease, which may result in bronzing of the skin, hypoglycemia, and low electrolyte levels in the blood.

Attributions

  • Hormonal Regulation of the Excretory System
    • "Boundless." http://www.boundless.com/. Boundless Learning CC BY-SA 3.0.
    • "renin." http://en.wiktionary.org/wiki/renin. Wiktionary CC BY-SA 3.0.
    • "aquaporin." http://en.wiktionary.org/wiki/aquaporin. Wiktionary CC BY-SA 3.0.
    • "electrolyte." http://en.wiktionary.org/wiki/electrolyte. Wiktionary CC BY-SA 3.0.
    • "aldosterone." http://en.wiktionary.org/wiki/aldosterone. Wiktionary CC BY-SA 3.0.
    • "mineralocorticoid." http://en.wiktionary.org/wiki/mineralocorticoid. Wiktionary CC BY-SA 3.0.
    • "OpenStax College, Biology. October 17, 2013." http://cnx.org/content/m44777/latest/?collection=col11448/latest. OpenStax CNX CC BY 3.0.
    • "osmoreceptor." http://en.wikipedia.org/wiki/osmoreceptor. Wikipedia CC BY-SA 3.0.
    • "antidiuretic hormone." http://en.wiktionary.org/wiki/antidiuretic_hormone. Wiktionary CC BY-SA 3.0.
    • "OpenStax College, Regulation of Body Processes. October 17, 2013." http://cnx.org/content/m44777/latest/Figure_37_03_01.jpg. OpenStax CNX CC BY 3.0.
  • Hormonal Regulation of the Reproductive System
    • "Boundless." http://www.boundless.com/. Boundless Learning CC BY-SA 3.0.
    • "GnRH." http://en.wikipedia.org/wiki/GnRH. Wikipedia CC BY-SA 3.0.
    • "Follicle-stimulating hormone." http://en.wikipedia.org/wiki/Follicle-stimulating_hormone%23Effects_in_males. Wikipedia CC BY-SA 3.0.
    • "gonadotropin-releasing hormone." http://en.wikipedia.org/wiki/gonadotropin-releasing%20hormone. Wikipedia CC BY-SA 3.0.
    • "prolactin." http://en.wiktionary.org/wiki/prolactin. Wiktionary CC BY-SA 3.0.
    • "luteinizing hormone." http://en.wiktionary.org/wiki/luteinizing_hormone. Wiktionary CC BY-SA 3.0.
    • "androgen." http://en.wiktionary.org/wiki/androgen. Wiktionary CC BY-SA 3.0.
    • "gonad." http://en.wiktionary.org/wiki/gonad. Wiktionary CC BY-SA 3.0.
    • "inhibin." http://en.wiktionary.org/wiki/inhibin. Wiktionary CC BY-SA 3.0.
    • "OpenStax College, Biology. October 17, 2013." http://cnx.org/content/m44777/latest/?collection=col11448/latest. OpenStax CNX CC BY 3.0.
    • "follicle stimulating hormone." http://en.wiktionary.org/wiki/follicle_stimulating_hormone. Wiktionary CC BY-SA 3.0.
    • "Hypothalamus pituitary testicles axis." http://en.wikipedia.org/wiki/File:Hypothalamus_pituitary_testicles_axis.png. Wikipedia CC BY-SA.
    • "OpenStax College, Regulation of Body Processes. October 17, 2013." http://cnx.org/content/m44777/latest/Figure_37_03_03.jpg. OpenStax CNX CC BY 3.0.
  • Hormonal Regulation of Metabolism
    • "Boundless." http://www.boundless.com/. Boundless Learning CC BY-SA 3.0.
    • "triiodothyronine." http://en.wiktionary.org/wiki/triiodothyronine. Wiktionary CC BY-SA 3.0.
    • "hypoglycemia." http://en.wiktionary.org/wiki/hypoglycemia. Wiktionary CC BY-SA 3.0.
    • "hypothyroidism." http://en.wiktionary.org/wiki/hypothyroidism. Wiktionary CC BY-SA 3.0.
    • "gluconeogenesis." http://en.wiktionary.org/wiki/gluconeogenesis. Wiktionary CC BY-SA 3.0.
    • "thyroxine." http://en.wiktionary.org/wiki/thyroxine. Wiktionary CC BY-SA 3.0.
    • "glycogen." http://en.wiktionary.org/wiki/glycogen. Wiktionary CC BY-SA 3.0.
    • "OpenStax College, Biology. October 17, 2013." http://cnx.org/content/m44777/latest/?collection=col11448/latest. OpenStax CNX CC BY 3.0.
    • "hyperthyroidism." http://en.wiktionary.org/wiki/hyperthyroidism. Wiktionary CC BY-SA 3.0.
    • "glucagon." http://en.wiktionary.org/wiki/glucagon. Wiktionary CC BY-SA 3.0.
    • "glycogenolysis." http://en.wiktionary.org/wiki/glycogenolysis. Wiktionary CC BY-SA 3.0.
    • "insulin." http://en.wiktionary.org/wiki/insulin. Wiktionary CC BY-SA 3.0.
    • "OpenStax College, Regulation of Body Processes. October 17, 2013." http://cnx.org/content/m44777/latest/Figure_37_03_05.png. OpenStax CNX CC BY 3.0.
    • "OpenStax College, Regulation of Body Processes. October 17, 2013." http://cnx.org/content/m44777/latest/Figure_37_03_04.jpg. OpenStax CNX CC BY 3.0.
  • Hormonal Control of Blood Calcium Levels
    • "Boundless." http://www.boundless.com/. Boundless Learning CC BY-SA 3.0.
    • "OpenStax College, Biology. October 17, 2013." http://cnx.org/content/m44777/latest/?collection=col11448/latest. OpenStax CNX CC BY 3.0.
    • "osteoblast." http://en.wiktionary.org/wiki/osteoblast. Wiktionary CC BY-SA 3.0.
    • "hyperparathyroidism." http://en.wiktionary.org/wiki/hyperparathyroidism. Wiktionary CC BY-SA 3.0.
    • "calcitonin." http://en.wiktionary.org/wiki/calcitonin. Wiktionary CC BY-SA 3.0.
    • "hypoparathyroidism." http://en.wiktionary.org/wiki/hypoparathyroidism. Wiktionary CC BY-SA 3.0.
    • "calcitriol." http://en.wiktionary.org/wiki/calcitriol. Wiktionary CC BY-SA 3.0.
    • "osteoclast." http://en.wiktionary.org/wiki/osteoclast. Wiktionary CC BY-SA 3.0.
    • "parathyroid hormone." http://en.wiktionary.org/wiki/parathyroid_hormone. Wiktionary CC BY-SA 3.0.
    • "OpenStax College, Regulation of Body Processes. October 17, 2013." http://cnx.org/content/m44777/latest/Figure_37_03_06.jpg. OpenStax CNX CC BY 3.0.
  • Hormonal Regulation of Growth
    • "Boundless." http://www.boundless.com/. Boundless Learning CC BY-SA 3.0.
    • "OpenStax College, Biology. October 17, 2013." http://cnx.org/content/m44777/latest/?collection=col11448/latest. OpenStax CNX CC BY 3.0.
    • "Growth hormone." http://en.wikipedia.org/wiki/Growth_hormone%23Function. Wikipedia CC BY-SA 3.0.
    • "growth hormone." http://en.wiktionary.org/wiki/growth_hormone. Wiktionary CC BY-SA 3.0.
    • "somatostatin." http://en.wiktionary.org/wiki/somatostatin. Wiktionary CC BY-SA 3.0.
    • "gigantism." http://en.wiktionary.org/wiki/gigantism. Wiktionary CC BY-SA 3.0.
    • "OpenStax College, Regulation of Body Processes. October 17, 2013." http://cnx.org/content/m44777/latest/Figure_37_03_07.png. OpenStax CNX CC BY 3.0.
  • Hormonal Regulation of Stress
    • "Boundless." http://www.boundless.com/. Boundless Learning CC BY-SA 3.0.
    • "OpenStax College, Biology. October 17, 2013." http://cnx.org/content/m44777/latest/?collection=col11448/latest. OpenStax CNX CC BY 3.0.
    • "catecholamine." http://en.wiktionary.org/wiki/catecholamine. Wiktionary CC BY-SA 3.0.
    • "norepinephrine." http://en.wiktionary.org/wiki/norepinephrine. Wiktionary CC BY-SA 3.0.
    • "adrenocorticotropic hormone." http://en.wiktionary.org/wiki/adrenocorticotropic_hormone. Wiktionary CC BY-SA 3.0.
    • "epinephrine." http://en.wiktionary.org/wiki/epinephrine. Wiktionary CC BY-SA 3.0.
    • "mineralocorticoid." http://en.wiktionary.org/wiki/mineralocorticoid. Wiktionary CC BY-SA 3.0.
    • "corticosteroid." http://en.wiktionary.org/wiki/corticosteroid. Wiktionary CC BY-SA 3.0.
    • "glucocorticoid." http://en.wiktionary.org/wiki/glucocorticoid. Wiktionary CC BY-SA 3.0.
    • "Gato enervado pola presencia dun can." http://en.wikipedia.org/wiki/File:Gato_enervado_pola_presencia_dun_can.jpg. Wikipedia CC BY.

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37.4: Regulation of Hormone Production
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