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Anatomy & Physiology 2e: 17.9 The Pancreas

Anatomy & Physiology 2e
17.9 The Pancreas
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table of contents
  1. Cover
  2. Title Page
  3. Copyright
  4. Table Of Contents
  5. Chapter 1. An Introduction to the Human Body
    1. 1.0 Introduction
    2. 1.1 How Structure Determines Function
    3. 1.2 Structural Organization of the Human Body
    4. 1.3 Homeostasis
    5. 1.4 Anatomical Terminology
    6. 1.5 Medical Imaging
  6. Chapter 2. The Chemical Level of Organization
    1. 2.0 Introduction
    2. 2.1 Elements and Atoms: The Building Blocks of Matter
    3. 2.2 Chemical Bonds
    4. 2.3 Chemical Reactions
    5. 2.4 Inorganic Compounds Essential to Human Functioning
    6. 2.5 Organic Compounds Essential to Human Functioning
  7. Chapter 3. The Cellular Level of Organization
    1. 3.0 Introduction
    2. 3.1 The Cell Membrane
    3. 3.2 The Cytoplasm and Cellular Organelles
    4. 3.3 The Nucleus and DNA Replication
    5. 3.4 Protein Synthesis
    6. 3.5 Cell Growth and Division
    7. 3.6 Cellular Differentiation
  8. Chapter 4. The Tissue Level of Organization
    1. 4.0 Introduction
    2. 4.1 Types of Tissues
    3. 4.2 Epithelial Tissue
    4. 4.3 Connective Tissue Supports and Protects
    5. 4.4 Muscle Tissue
    6. 4.5 Nervous Tissue
    7. 4.6 Tissue Injury and Aging
  9. Chapter 5. The Integumentary System
    1. 5.0 Introduction
    2. 5.1 Layers of the Skin
    3. 5.2 Accessory Structures of the Skin
    4. 5.3 Functions of the Integumentary System
    5. 5.4 Diseases, Disorders, and Injuries of the Integumentary System
  10. Chapter 6. Bone Tissue and the Skeletal System
    1. 6.0 Introduction
    2. 6.1 The Functions of the Skeletal System
    3. 6.2 Bone Classification
    4. 6.3 Bone Structure
    5. 6.4 Bone Formation and Development
    6. 6.5 Fractures: Bone Repair
    7. 6.6 Exercise, Nutrition, Hormones, and Bone Tissue
    8. 6.7 Calcium Homeostasis: Interactions of the Skeletal System and Other Organ Systems
  11. Chapter 7. Axial Skeleton
    1. 7.0 Introduction
    2. 7.1 Divisions of the Skeletal System
    3. 7.2 Bone Markings
    4. 7.3 The Skull
    5. 7.4 The Vertebral Column
    6. 7.5 The Thoracic Cage
    7. 7.6 Embryonic Development of the Axial Skeleton
  12. Chapter 8. The Appendicular Skeleton
    1. 8.0 Introduction
    2. 8.1 The Pectoral Girdle
    3. 8.2 Bones of the Upper Limb
    4. 8.3 The Pelvic Girdle and Pelvis
    5. 8.4 Bones of the Lower Limb
    6. 8.5 Development of the Appendicular Skeleton
  13. Chapter 9. Joints
    1. 9.0 Introduction
    2. 9.1 Classification of Joints
    3. 9.2 Fibrous Joints
    4. 9.3 Cartilaginous Joints
    5. 9.4 Synovial Joints
    6. 9.5 Types of Body Movements
    7. 9.6 Anatomy of Selected Synovial Joints
    8. 9.7 Development of Joints
  14. Chapter 10. Muscle Tissue
    1. 10.0 Introduction
    2. 10.1 Overview of Muscle Tissues
    3. 10.2 Skeletal Muscle
    4. 10.3 Muscle Fiber Excitation, Contraction, and Relaxation
    5. 10.4 Nervous System Control of Muscle Tension
    6. 10.5 Types of Muscle Fibers
    7. 10.6 Exercise and Muscle Performance
    8. 10.7 Smooth Muscle Tissue
    9. 10.8 Development and Regeneration of Muscle Tissue
  15. Chapter 11. The Muscular System
    1. 11.0 Introduction
    2. 11.1 Describe the roles of agonists, antagonists and synergists
    3. 11.2 Explain the organization of muscle fascicles and their role in generating force
    4. 11.3 Explain the criteria used to name skeletal muscles
    5. 11.4 Axial Muscles of the Head Neck and Back
    6. 11.5 Axial muscles of the abdominal wall and thorax
    7. 11.6 Muscles of the Pectoral Girdle and Upper Limbs
    8. 11.7 Appendicular Muscles of the Pelvic Girdle and Lower Limbs
  16. Chapter 12. The Nervous System and Nervous Tissue
    1. 12.0 Introduction
    2. 12.1 Structure and Function of the Nervous System
    3. 12.2 Nervous Tissue
    4. 12.3 The Function of Nervous Tissue
    5. 12.4 Communication Between Neurons
    6. 12.5 The Action Potential
  17. Chapter 13. The Peripheral Nervous System
    1. 13.0 Introduction
    2. 13.1 Sensory Receptors
    3. 13.2 Ganglia and Nerves
    4. 13.3 Spinal and Cranial Nerves
    5. 13.4 Relationship of the PNS to the Spinal Cord of the CNS
    6. 13.5 Ventral Horn Output and Reflexes
    7. 13.6 Testing the Spinal Nerves (Sensory and Motor Exams)
    8. 13.7 The Cranial Nerve Exam
  18. Chapter 14. The Central Nervous System
    1. 14.0 Introduction
    2. 14.1 Embryonic Development
    3. 14.2 Blood Flow the meninges and Cerebrospinal Fluid Production and Circulation
    4. 14.3 The Brain and Spinal Cord
    5. 14.4 The Spinal Cord
    6. 14.5 Sensory and Motor Pathways
  19. Chapter 15. The Special Senses
    1. 15.0 Introduction
    2. 15.1 Taste
    3. 15.2 Smell
    4. 15.3 Hearing
    5. 15.4 Equilibrium
    6. 15.5 Vision
  20. Chapter 16. The Autonomic Nervous System
    1. 16.0 Introduction
    2. 16.1 Divisions of the Autonomic Nervous System
    3. 16.2 Autonomic Reflexes and Homeostasis
    4. 16.3 Central Control
    5. 16.4 Drugs that Affect the Autonomic System
  21. Chapter 17. The Endocrine System
    1. 17.0 Introduction
    2. 17.1 An Overview of the Endocrine System
    3. 17.2 Hormones
    4. 17.3 The Pituitary Gland and Hypothalamus
    5. 17.4 The Thyroid Gland
    6. 17.5 The Parathyroid Glands
    7. 17.6 The Adrenal Glands
    8. 17.7 The Pineal Gland
    9. 17.8 Gonadal and Placental Hormones
    10. 17.9 The Pancreas
    11. 17.10 Organs with Secondary Endocrine Functions
    12. 17.11 Development and Aging of the Endocrine System
  22. Chapter 18. The Cardiovascular System: Blood
    1. 18.0 Introduction
    2. 18.1 Functions of Blood
    3. 18.2 Production of the Formed Elements
    4. 18.3 Erythrocytes
    5. 18.4 Leukocytes and Platelets
    6. 18.5 Hemostasis
    7. 18.6 Blood Typing
  23. Chapter 19. The Cardiovascular System: The Heart
    1. 19.0 Introduction
    2. 19.1 Heart Anatomy
    3. 19.2 Cardiac Muscle and Electrical Activity
    4. 19.3 Cardiac Cycle
    5. 19.4 Cardiac Physiology
    6. 19.5 Development of the Heart
  24. Chapter 20. The Cardiovascular System: Blood Vessels and Circulation
    1. 20.0 Introduction
    2. 20.1 Structure and Function of Blood Vessels
    3. 20.2 Blood Flow, Blood Pressure, and Resistance
    4. 20.3 Capillary Exchange
    5. 20.4 Homeostatic Regulation of the Vascular System
    6. 20.5 Circulatory Pathways
    7. 20.6 Development of Blood Vessels and Fetal Circulation
  25. Chapter 21. The Lymphatic and Immune System
    1. 21.0 Introduction
    2. 21.1 Anatomy of the Lymphatic and Immune Systems
    3. 21.2 Barrier Defenses and the Innate Immune Response
    4. 21.3 The Adaptive Immune Response: T lymphocytes and Their Functional Types
    5. 21.4 The Adaptive Immune Response: B-lymphocytes and Antibodies
    6. 21.5 The Immune Response against Pathogens
    7. 21.6 Diseases Associated with Depressed or Overactive Immune Responses
    8. 21.7 Transplantation and Cancer Immunology
  26. Chapter 22. The Respiratory System
    1. 22.0 Introduction
    2. 22.1 Organs and Structures of the Respiratory System
    3. 22.2 The Lungs
    4. 22.3 The Process of Breathing
    5. 22.4 Gas Exchange
    6. 22.5 Transport of Gases
    7. 22.6 Modifications in Respiratory Functions
    8. 22.7 Embryonic Development of the Respiratory System
  27. Chapter 23. The Digestive System
    1. 23.0 Introduction
    2. 23.1 Overview of the Digestive System
    3. 23.2 Digestive System Processes and Regulation
    4. 23.3 The Mouth, Pharynx, and Esophagus
    5. 23.4 The Stomach
    6. 23.5 Accessory Organs in Digestion: The Liver, Pancreas, and Gallbladder
    7. 23.6 The Small and Large Intestines
    8. 23.7 Chemical Digestion and Absorption: A Closer Look
  28. Chapter 24. Metabolism and Nutrition
    1. 24.0 Introduction
    2. 24.1 Overview of Metabolic Reactions
    3. 24.2 Carbohydrate Metabolism
    4. 24.3 Lipid Metabolism
    5. 24.4 Protein Metabolism
    6. 24.5 Metabolic States of the Body
    7. 24.6 Energy and Heat Balance
    8. 24.7 Nutrition and Diet
  29. Chapter 25. The Urinary System
    1. 25.0 Introduction
    2. 25.1 Internal and External Anatomy of the Kidney
    3. 25.2 Microscopic Anatomy of the Kidney: Anatomy of the Nephron
    4. 25.3 Physiology of Urine Formation: Overview
    5. 25.4 Physiology of Urine Formation: Glomerular Filtration
    6. 25.5 Physiology of Urine Formation: Tubular Reabsorption and Secretion
    7. 25.6 Physiology of Urine Formation: Medullary Concentration Gradient
    8. 25.7 Physiology of Urine Formation: Regulation of Fluid Volume and Composition
    9. 25.8 Urine Transport and Elimination
    10. 25.9 The Urinary System and Homeostasis
  30. Chapter 26. Fluid, Electrolyte, and Acid-Base Balance
    1. 26.0 Introduction
    2. 26.1 Body Fluids and Fluid Compartments
    3. 26.2 Water Balance
    4. 26.3 Electrolyte Balance
    5. 26.4 Acid-Base Balance
    6. 26.5 Disorders of Acid-Base Balance
  31. Chapter 27. The Sexual Systems
    1. 27.0 Introduction
    2. 27.1 Anatomy of Sexual Systems
    3. 27.2 Development of Sexual Anatomy
    4. 27.3 Physiology of the Female Sexual System
    5. 27.4 Physiology of the Male Sexual System
    6. 27.5 Physiology of Arousal and Orgasm
  32. Chapter 28. Development and Inheritance
    1. 28.0 Introduction
    2. 28.1 Fertilization
    3. 28.2 Embryonic Development
    4. 28.3 Fetal Development
    5. 28.4 Maternal Changes During Pregnancy, Labor, and Birth
    6. 28.5 Adjustments of the Infant at Birth and Postnatal Stages
    7. 28.6 Lactation
    8. 28.7 Patterns of Inheritance
  33. Creative Commons License
  34. Recommended Citations
  35. Versioning

17.9 The Pancreas

Learning Objectives

By the end of this section, you will be able to:

Explain the role of the pancreatic endocrine cells in the regulation of blood glucose

  • Describe the location and structure of the pancreas, and the morphology and function of the pancreatic islets
  • Compare and contrast the function and regulation of insulin and glucagon

The pancreas is a long, slender organ, most of which is located posterior to the bottom half of the stomach (Figure 17.9.1). Although it is primarily an exocrine gland, secreting a variety of digestive enzymes, the pancreas also has endocrine cells. Its pancreatic islets—clusters of cells formerly known as the islets of Langerhans—secrete the hormones glucagon, insulin, somatostatin, and pancreatic polypeptide (PP).

This diagram shows the anatomy of the pancreas. The left, larger side of the pancreas is seated within the curve of the duodenum of the small intestine. The smaller, rightmost tip of the pancreas is located near the spleen. The splenic artery is seen travelling to the spleen, however, it has several branches connecting to the pancreas. An interior view of the pancreas shows that the pancreatic duct is a large tube running through the center of the pancreas. It branches throughout its length in to several horseshoe- shaped pockets of acinar cells. These cells secrete digestive enzymes, which travel down the bile duct and into the small intestine. There are also small pancreatic islets scattered throughout the pancreas. The pancreatic islets secrete the pancreatic hormones insulin and glucagon into the splenic artery. An inset micrograph shows that the pancreatic islets are small discs of tissue consisting of a thin, outer ring called the exocrine acinus, a thicker, inner ring of beta cells and a central circle of alpha cells.
Figure 17.9.1 – Pancreas Pancreas endocrine function involves the secretion of insulin (produced by beta cells) and glucagon (produced by alpha cells) within the pancreatic islets. These two hormones regulate the rate of glucose metabolism in the body. The micrograph reveals pancreatic islets. LM × 760. Also shown are the exocrine acinar cells. (Micrograph provided by the Regents of University of Michigan Medical School © 2012.

External Website

QR Code representing a URL

View the University of Michigan WebScope at http://141.214.65.171/Histology/Digestive%20System/Liver%20and%20Pancreas/188B_HISTO_40X.svs/view.apml to explore the tissue sample in greater detail.

Cells and Secretions of the Pancreatic Islets

The pancreatic islets each contain four varieties of cells:

  • The alpha cell produces the hormone glucagon and makes up approximately 20 percent of each islet. Low blood glucose levels stimulate the release of glucagon.
  • The beta cell produces the hormone insulin and makes up approximately 75 percent of each islet. Elevated blood glucose levels stimulate the release of insulin.
  • The delta cell accounts for four percent of the islet cells and secretes the peptide hormone somatostatin. Recall that somatostatin is also released by the hypothalamus, stomach and intestines. An inhibiting hormone, pancreatic somatostatin inhibits the release of both glucagon and insulin.
  • The pancreatic polypeptide cell (PP cell) accounts for about one percent of islet cells and secretes the pancreatic polypeptide hormone. It is thought to play a role in appetite, as well as in the regulation of pancreatic exocrine and endocrine secretions. Pancreatic polypeptide released following a meal may reduce further food consumption; however, it is also released in response to fasting.

Regulation of Blood Glucose Levels by Insulin and Glucagon

Glucose is utilized in cellular respiration as a fuel for cells of the body. The body derives glucose from the breakdown of the carbohydrate-containing foods and drinks we consume. Glucose not immediately taken up by cells for fuel can be stored by the liver and muscles as glycogen, or converted to triglycerides and stored in the adipose tissue. Hormones regulate both the storage and the utilization of glucose as required. Receptors located in the pancreas sense blood glucose levels, and subsequently the pancreatic cells secrete glucagon or insulin to maintain appropriate blood glucose.

Glucagon

Receptors in the pancreas can sense the decline in blood glucose levels, such as during periods of fasting or during prolonged labor or exercise (Figure 17.9.2). In response, the alpha cells of the pancreas secrete the hormone glucagon, which has several effects:

  • Glucagon stimulates the liver to convert its stores of glycogen back into glucose. This response is known as glycogenolysis. The glucose is then released into the circulation for use by cells throughout the body.
  • Glucagon stimulates the liver to take up amino acids from the blood and convert them into glucose. This response is known as gluconeogenesis.
  • Glucagon stimulates lipolysis, the breakdown of stored triglycerides into free fatty acids and glycerol. Some of the free glycerol released into the bloodstream travels to the liver, which converts the glycerol into glucose. This is also a form of gluconeogenesis.

Taken together, these actions increase blood glucose levels. The activity of glucagon is regulated through a negative feedback mechanism; rising blood glucose levels inhibit further glucagon production and secretion.

This diagram shows the homeostatic regulation of blood glucose levels. Blood glucose concentration is tightly maintained between 70 milligrams per deciliter and 110 milligrams per deciliter. If blood glucose concentration rises above this range (hyperglycemia), insulin is released from the pancreas. Insulin triggers body cells to take up glucose from the blood and utilize it in cellular respiration. Insulin also inhibits glycogenolysis, in that glucose is removed from the blood and stored as glycogen in the liver. Insulin also inhibits gluconeogenesis, in that amino acids and free glycerol are not converted to glucose in the ER. If blood glucose concentration drops below this range, glucagon is released, which stimulates body cells to release glucose into the blood. All of these actions cause blood glucose concentration to decrease. When blood glucose concentration is low (hypoglycemia), alpha cells of the pancreas release glucagon. Glucagon inhibits body cells from taking up glucose from the blood and utilizing it in cellular respiration. Glucagon also stimulates glycogenolysis, in that glycogen in the liver is broken down into glucose and released into the blood. Glucagon also stimulates glucogenogenesis, in that amino acids and free glycerol are converted to glucose in the ER and released into the blood. All of these actions cause blood glucose concentrations to increase.
Figure 17.9.2 – Homeostatic Regulation of Blood Glucose Levels: Blood glucose concentration is tightly maintained between 70 mg/dL and 110 mg/dL. If blood glucose concentration rises above this range, insulin is released, which stimulates body cells to remove glucose from the blood. If blood glucose concentration drops below this range, glucagon is released, which stimulates body cells to release glucose into the blood.

Insulin

The primary function of insulin is to facilitate the uptake of glucose into body cells. Red blood cells, as well as cells of the brain, liver, kidneys, and the lining of the small intestine, do not have insulin receptors on their cell membranes and do not require insulin for glucose uptake. Although all other body cells do require insulin if they are to take glucose from the bloodstream, skeletal muscle cells and adipose cells are the primary targets of insulin.

The presence of food in the intestine triggers the release of gastrointestinal tract hormones such as glucose-dependent insulinotropic peptide (previously known as gastric inhibitory peptide). This is in turn the initial trigger for insulin production and secretion by the beta cells of the pancreas. Once nutrient absorption occurs, the resulting surge in blood glucose levels further stimulates insulin secretion.

Precisely how insulin facilitates glucose uptake is not entirely clear. However, insulin appears to activate a tyrosine kinase receptor, triggering the phosphorylation of many substrates within the cell. These multiple biochemical reactions converge to support the movement of intracellular vesicles containing facilitative glucose transporters to the cell membrane. In the absence of insulin, these transport proteins are normally recycled slowly between the cell membrane and cell interior. Insulin triggers the rapid movement of a pool of glucose transporter vesicles to the cell membrane, where they fuse and expose the glucose transporters to the extracellular fluid. The transporters then move glucose by facilitated diffusion into the cell interior.

External Website

QR Code representing a URL

Visit this link to view an animation describing the location and function of the pancreas. What goes wrong in the function of insulin in type 2 diabetes? Note, this animation mis-represents the glucose transport mechanism which here is simplified as a “gated” mechanism.

Insulin also reduces blood glucose levels by stimulating glycolysis, the metabolism of glucose for generation of ATP. Moreover, it stimulates the liver to convert excess glucose into glycogen for storage, and it inhibits enzymes involved in glycogenolysis and gluconeogenesis. Finally, insulin promotes triglyceride and protein synthesis. The secretion of insulin is regulated through a negative feedback mechanism. As blood glucose levels decrease, further insulin release is inhibited.

The pancreatic hormones are summarized in Table 17.7.

Hormones of the Pancreas (Table 17.7)
Associated hormonesChemical classEffect
Insulin (beta cells)ProteinReduces blood glucose levels
Glucagon (alpha cells)ProteinIncreases blood glucose levels
Somatostatin (delta cells)ProteinInhibits insulin and glucagon release
Pancreatic polypeptide (PP cells)ProteinRole in appetite

Disorders of the…Endocrine System: Diabetes Mellitus

Dysfunction of insulin production and secretion, as well as the target cells’ responsiveness to insulin, can lead to a condition called diabetes mellitus. As of 2012 the American Diabetes Association reports that diabetes mellitus has been diagnosed in more than 21 million people in the United States; more than 200,000 of those are children. It is estimated that more than 8 million additional adults have the condition but have not been diagnosed. In addition, approximately 86 million people in the US are estimated to have pre-diabetes, a condition in which blood glucose levels are abnormally high, but not yet high enough to be classified as diabetes.

There are two main forms of diabetes mellitus. Type 1 diabetes is an autoimmune disease affecting the beta cells of the pancreas. Certain genes are recognized to increase susceptibility. The beta cells of people with type 1 diabetes do not produce insulin; thus, synthetic insulin must be administered by injection or infusion. This form of diabetes accounts for less than five percent of all diabetes cases.

Type 2 diabetes accounts for approximately 95 percent of all cases. Factors such as family history, ethnicity, age, and the presence of pre-diabetes greatly increase a person’s risk. Often, people with type 2 diabetes are overweight or obese, although weight is not the only risk factor. In type 2 diabetes, cells become resistant to the effects of insulin. In response, the pancreas increases its insulin secretion, but over time, the beta cells become exhausted. In many cases, type 2 diabetes can be reversed by moderate weight loss, regular physical activity, and consumption of a healthy diet; however, if blood glucose levels cannot be controlled, the type 2 diabetic may eventually require synthetic insulin injections.

Two of the early symptoms of the onset of diabetes are excessive urination and excessive thirst. These symptoms demonstrate how the out-of-control levels of glucose in the blood affect kidney function. The kidneys are responsible for filtering the blood. Excessive blood glucose draws water into the urine, and as a result the person eliminates an abnormally large quantity of urine. The use of body water to dilute the urine leaves the body dehydrated, and so the person is unusually and continually thirsty. The person may also experience persistent hunger because the body cells are unable to access the glucose in the bloodstream.

Over time, persistently high levels of glucose in the blood injure tissues throughout the body, especially those of the blood vessels and nerves. Inflammation and injury of the lining of arteries lead to atherosclerosis and an increased risk of heart attack and stroke. Damage to the microscopic blood vessels of the kidney impairs kidney function and can lead to kidney failure. Damage to blood vessels that serve the retina can lead to blindness. Blood vessel damage also reduces circulation to the limbs, whereas nerve damage leads to a loss of sensation, called neuropathy, particularly in the hands and feet. Together, these changes increase the risk of injury, infection, and tissue death (necrosis), contributing to a high rate of toe, foot, and lower leg amputations in people with diabetes. Uncontrolled diabetes can also lead to a dangerous form of metabolic acidosis called ketoacidosis. Deprived of glucose, cells increasingly rely on fat stores for fuel. However, in a glucose-deficient state, the liver is forced to use an alternative lipid metabolism pathway that results in the increased production of ketone bodies (or ketones), which are acidic. The build-up of ketones in the blood causes ketoacidosis, which—if left untreated—may lead to a life-threatening “diabetic coma.” Together, these complications make diabetes the seventh leading cause of death in the United States (2010, American Diabetes Association).

Diabetes is diagnosed when lab tests reveal that blood glucose levels are higher than normal, a condition called hyperglycemia. The treatment of diabetes depends on the type, the severity of the condition, and the ability of the patient to make lifestyle changes. As noted earlier, moderate weight loss, regular physical activity, and consumption of a healthful diet can reduce blood glucose levels in type 2 diabetics. Some patients with type 2 diabetes may be unable to control their disease with these lifestyle changes, and will require medication. Historically, the first-line treatment of type 2 diabetes was insulin. Research advances have resulted in alternative options, including medications that enhance pancreatic function.

External Website

QR Code representing a URL

Visit this link to view an animation describing the role of insulin and the pancreas in diabetes.

Chapter Review

The pancreas has both exocrine and endocrine functions. Alpha cells of the pancreas produce glucagon, while beta cells produce insulin. Insulin and glucagon are involved in the regulation of glucose metabolism. Insulin is produced by the beta cells in response to high blood glucose levels. It enhances glucose uptake and utilization by target cells, as well as the storage of excess glucose for later use. Dysfunction of the production of insulin or target cell resistance to the effects of insulin causes diabetes mellitus, a disorder characterized by high blood glucose levels. The hormone glucagon is produced and secreted by the alpha cells of the pancreas in response to low blood glucose levels. Glucagon stimulates mechanisms that increase blood glucose levels, such as the catabolism of glycogen into glucose.

Interactive Link Questions

Visit this link to view an animation describing the location and function of the pancreas. What goes wrong in type 2 diabetes?

Insulin receptors no longer function.

Review Questions

An interactive H5P element has been excluded from this version of the text. You can view it online here:
https://open.oregonstate.education/aandp/?p=787#h5p-346

An interactive H5P element has been excluded from this version of the text. You can view it online here:
https://open.oregonstate.education/aandp/?p=787#h5p-347

Critical Thinking Questions

1. What is the physiological consequence of the disease that destroys the beta cells of the pancreas?

2. Why is foot care extremely important for people with diabetes mellitus?

Glossary

alpha cell
pancreatic islet cell type that produces the hormone glucagon
beta cell
pancreatic islet cell type that produces the hormone insulin
delta cell
minor cell type in the pancreas that secretes the hormone somatostatin
diabetes mellitus
condition caused by destruction or dysfunction of the beta cells of the pancreas or cellular resistance to insulin that results in abnormally high blood glucose levels
glucagon
pancreatic hormone that stimulates the catabolism of glycogen to glucose, thereby increasing blood glucose levels
hyperglycemia
abnormally high blood glucose levels
insulin
pancreatic hormone that enhances the cellular uptake and utilization of glucose, thereby decreasing blood glucose levels
pancreas
organ with both exocrine and endocrine functions located posterior to the stomach that is important for digestion and the regulation of blood glucose
pancreatic islets
specialized clusters of pancreatic cells that have endocrine functions; also called islets of Langerhans
pancreatic polypeptide (PP) cell
minor cell type in the pancreas that secretes the hormone pancreatic polypeptide

Solutions

Answers for Critical Thinking Questions

  1. The beta cells produce the hormone insulin, which is important in the regulation of blood glucose levels. All insulin-dependent cells of the body require insulin in order to take up glucose from the bloodstream. Destruction of the beta cells would result in an inability to produce and secrete insulin, leading to abnormally high blood glucose levels and the disease called type 1 diabetes mellitus.
  2. Excessive blood glucose levels damage the blood vessels and nerves of the body’s extremities, increasing the risk for injury, infection, and tissue death. Loss of sensation to the feet means that a diabetic patient will not be able to feel foot trauma, such as from ill-fitting shoes. Even minor injuries commonly lead to infection, which , can progress to tissue death without proper care, requiring amputation.

Annotate

Next chapter
17.10 Organs with Secondary Endocrine Functions
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Anatomy and Physiology
Copyright © 2019 by Lindsay M. Biga, Sierra Dawson, Amy Harwell, Robin Hopkins, Joel Kaufmann, Mike LeMaster, Philip Matern, Katie Morrison-Graham, Devon Quick & Jon Runyeon

Anatomy & Physiology by Lindsay M. Biga, Sierra Dawson, Amy Harwell, Robin Hopkins, Joel Kaufmann, Mike LeMaster, Philip Matern, Katie Morrison-Graham, Devon Quick & Jon Runyeon is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License, except where otherwise noted.

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