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Fundamentals of Anatomy and Physiology: 14.9 The Endocrine Pancreas

Fundamentals of Anatomy and Physiology
14.9 The Endocrine Pancreas
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table of contents
  1. Cover
  2. Title Page
  3. Copyright
  4. Table Of Contents
  5. About the Authors
  6. Acknowledgments
  7. Preface
  8. Levels of Organisation, Homeostasis and Nomenclature
    1. 1.1 Overview of Anatomy and Physiology
    2. 1.2 Structural Organisation of the Human Body
    3. 1.3 Homeostasis
    4. 1.4 Anatomical Terminology
  9. Cells and Reproduction
    1. 2.1 Synthesis of Biological Macromolecules
    2. 2.2 Carbohydrates
    3. 2.3 Lipids
    4. 2.4 Protein
    5. 2.5 Nucleic Acid
    6. 2.6 The Cell Membrane
    7. 2.7 The Cytoplasm and Cellular Organelles
    8. 2.8 The Nucleus and DNA Replication
    9. 2.9 Protein Synthesis
    10. 2.10 Cell Growth and Division
    11. 2.11 Cellular Differentiation
  10. Tissues, Organs, Systems
    1. 3.1 Types of Tissues
    2. 3.2 Epithelial Tissue
    3. 3.3 Connective Tissue Supports and Protects
    4. 3.4 Muscle Tissue and Motion
    5. 3.5 Nervous Tissue Mediates Perception and Response
    6. 3.6 Tissue Injury and Ageing
  11. Integumentary System
    1. 4.1 Layers of the Skin
    2. 4.2 Accessory Structures of the Skin
    3. 4.3 Functions of the Integumentary System
    4. 4.4 Diseases, Disorders and Injuries of the Integumentary System
  12. Blood
    1. 5.1 An Overview of Blood
    2. 5.2 Production of the Formed Elements
    3. 5.3 Erythrocytes
    4. 5.4 Leukocytes and Platelets
    5. 5.5 Haemostasis
    6. 5.6 Blood Typing
  13. Cardiovascular System
    1. 6.1 Heart Anatomy
    2. 6.2 Cardiac Muscle and Electrical Activity
    3. 6.3 Cardiac Cycle
    4. 6.4 Cardiac Physiology
    5. 6.5 Development of the Heart
    6. 6.6 Structure and Function of Blood Vessels
    7. 6.7 Blood Flow, Blood Pressure and Resistance
    8. 6.8 Capillary Exchange
    9. 6.9 Homeostatic Regulation of the Vascular System
    10. 6.10 Circulatory Pathways
    11. 6.11 Development of Blood Vessels and Foetal Circulation
  14. Lymphatic System and Immunity
    1. 7.1 Anatomy of the Lymphatic and Immune Systems
    2. 7.2 Barrier Defences and the Innate Immune Response
    3. 7.3 The Adaptive Immune Response: T Lymphocytes and their Functional Types
    4. 7.4 The Adaptive Immune Response: B-Lymhocytes and Antibodies
    5. 7.5 The Immune Response Against Pathogens
    6. 7.6 Diseases Associated with Depressed or Overactive Immune Responses
    7. 7.7 Transplantation and Cancer Immunology
  15. Respiratory System
    1. 8.1 Organs and Structures of the Respiratory System
    2. 8.2 The Lungs
    3. 8.3 The Process of Breathing
    4. 8.4 Gas Exchange
    5. 8.5 Transport of Gases
    6. 8.6 Modifications in Respiratory Functions
    7. 8.7 Embryonic Development of the Respiratory System
  16. Muscle System
    1. 9.1 Overview of Muscle Tissues
    2. 9.2 Skeletal Muscle
    3. 9.3 Muscle Fibre Contraction and Relaxation
    4. 9.4 Nervous System Control of Muscle Tension
    5. 9.5 Types of Muscle Fibres
    6. 9.6 Exercise and Muscle Performance
    7. 9.7 Cardiac Muscle Tissue
    8. 9.8 Smooth Muscle
    9. 9.9 Development and Regeneration of Muscle Tissue
  17. Skeletal System
    1. 10.1 The Functions of the Skeletal System
    2. 10.2 Bone Classification
    3. 10.3 Bone Structure
    4. 10.4 Bone Formation and Development
    5. 10.5 Fractures: Bone Repair
    6. 10.6 Exercise, Nutrition, Hormones and Bone Tissue
    7. 10.7 Calcium Homeostasis: Interactions of the Skeletal System and Other Organ Systems
    8. 10.8 Divisions of the Skeletal System
    9. 10.9 The Skull
    10. 10.10 The Vertebral Column
    11. 10.11 The Thoracic Cage
    12. 10.12 Embryonic Development of the Axial Skeleton
  18. Musculoskeletal System
    1. 11.1 The Pectoral Girdle
    2. 11.2 Bones of the Upper Limb
    3. 11.3 The Pelvic Girdle and Pelvis
    4. 11.4 Bones of the Lower Limb
    5. 11.5 Development of the Appendicular Skeleton
    6. 11.6 Classification of Joints
    7. 11.7 Fibrous Joints
    8. 11.8 Cartilaginous Joints
    9. 11.9 Synovial Joints
    10. 11.10 Types of Body Movements
    11. 11.11 Anatomy of Selected Synovial Joints
    12. 11.12 Development of Joints
  19. Digestive System
    1. 12.1 Overview of the Digestive System
    2. 12.2 Digestive System Processes and Regulation
    3. 12.3 The Mouth, Pharynx and Oesophagus
    4. 12.4 The Stomach
    5. 12.5 The Small and Large Intestines
    6. 12.6 Accessory Organs in Digestion: the Liver, Pancreas and Gallbladder
    7. 12.7 Chemical Digestion and Absorption
  20. Nervous System
    1. 13.1 Basic Structure and Function of the Nervous System
    2. 13.2 Nervous Tissue
    3. 13.3 The Function of Nervous Tissue
    4. 13.4 The Action Potential
    5. 13.5 Communication between Neurons
    6. 13.6 The Embyrologic Perspective
    7. 13.7 The Central Nervous System
    8. 13.8 Circulation and the Central Nervous System
    9. 13.9 The Peripheral Nervous System
    10. 13.10 Sensory Perception
    11. 13.11 Central Processing
    12. 13.12 Motor Responses
  21. Endocrine System
    1. 14.1 An Overview of the Endocrine System
    2. 14.2 Hormones
    3. 14.3 The Pituitary Gland and Hypothalamus
    4. 14.4 The Thyroid Gland
    5. 14.5 The Parathyroid Glands
    6. 14.6 The Adrenal Glands
    7. 14.7 The Pineal Gland
    8. 14.8 Gonadal and Placental Hormones
    9. 14.9 The Endocrine Pancreas
    10. 14.10 Organs with Secondary Endocrine Functions
    11. 14.11 Development and Ageing of the Endocrine System
  22. Reproductive System
    1. 15.1 Anatomy and Physiology of the Male Reproductive System
    2. 15.2 Anatomy and Physiology of the Female Reproductive System
    3. 15.3 Development of the Male and Female Reproductive Systems
  23. Pregnancy and Human Development
    1. 16.1 Fertilisation
    2. 16.2 Embryonic Development
    3. 16.3 Foetal Development
  24. Urinary System
    1. 17.1 Physical Characteristics of Urine
    2. 17.2 Gross Anatomy of Urine Transport
    3. 17.3 Gross Anatomy of the Kidney
    4. 17.4 Microscopic Anatomy of the Kidney
    5. 17.5 Physiology of Urine Formation
    6. 17.6 Tubular Reabsorption
    7. 17.7 Regulation of Renal Blood Flow
    8. 17.8 Endocrine Regulation of Kidney Function
    9. 17.9 Regulation of Fluid Volume and Composition
    10. 17.10 The Urinary System and Homeostasis
    11. 17.11 Body Fluids and Fluid Compartments
    12. 17.12 Water Balance
    13. 17.13 Electrolyte Balance
    14. 17.14 Acid-Base Balance
    15. 17.15 Disorders of Acid-Base Balance
  25. Appendix A: Unit Measurements and Calculations
  26. Appendix B: Chemical Abbreviations
  27. Glossary
  28. Bibliography

14.9 The Endocrine Pancreas

Learning Objectives

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

  • Describe the location and structure of the pancreas, and the morphology and function of the pancreatic islets
  • Compare and contrast the functions 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 14.9.1). Although it is primarily an exocrine gland, secreting a variety of digestive enzymes, the pancreas has an endocrine function. Its pancreatic islets—clusters of cells formerly known as the islets of Langerhans—secrete the hormones glucagon, insulin, somatostatin and pancreatic polypeptide (PP) among others.

Diagram of pancreas
Figure 14.9.1. Pancreas. The pancreatic exocrine function involves the acinar cells secreting digestive enzymes that are transported into the small intestine by the pancreatic duct. Its 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 shows pancreatic islets. LM × 760. (Micrograph provided by the Regents of University of Michigan Medical School © 2012).

Cells and Secretions of the Pancreatic Islets

The pancreatic islets each contain five main varieties of cells:

  1. The alpha cell produces the hormone glucagon and makes up approximately 20 percent of each islet. Glucagon plays an important role in blood glucose regulation; low blood glucose levels stimulate its release.
  2. The beta cell produces the hormones insulin and amylin and makes up approximately 75 percent of each islet. Elevated blood glucose levels stimulate the release of insulin.
  3. The delta cell accounts for about four percent of the islet cells and secretes the peptide hormone somatostatin. Recall that somatostatin is also released by the hypothalamus (as GHIH), and the stomach and intestines also secrete it. An inhibiting hormone, pancreatic somatostatin inhibits the release of both glucagon and insulin.
  4. The gamma 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.
  5. The epsilon cell produces the hormone ghrelin and accounts for less than 1 percent of islet cells.

Regulation of Blood Glucose Levels by Insulin and Glucagon

Glucose is required for cellular respiration and is the preferred fuel for all body cells. 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 utilisation of glucose as required. Receptors located in the pancreas sense blood glucose levels, and subsequently the pancreatic cells secrete glucagon or insulin to maintain normal levels.

Glucagon

Receptors in the pancreas can sense the decline in blood glucose levels, such as during periods of fasting or during prolonged labour or exercise (Figure 14.9.2). In response, the alpha cells of the pancreas secrete the hormone glucagon, which has several effects:

  • It 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 body cells.
  • It stimulates the liver to take up amino acids from the blood and convert them into glucose. This response is known as gluconeogenesis.
  • It 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 it 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.

Diagram of Homeostatic regulation of blood glucose levels
Figure 14.9.2. Homeostatic regulation of blood glucose levels. Blood glucose concentration is tightly maintained between 70 mg/dL and 110 mg/dL (or between 4.0 mmol/L and 7.8 mmol/L). 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.

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 summarised in Table 14.9.1.

Table 14.9.1. Hormones of the pancreas

Associated hormonesChemical classEffect
Glucagon (alpha cells)ProteinIncreases blood glucose levels
Insulin (beta cells)ProteinReduces blood glucose levels
Somatostatin (delta cells)ProteinInhibits insulin and glucagon release
Pancreatic polypeptide (gamma or PP cells)ProteinRole in appetite
Ghrelin (epsilon cells)

ProteinStimulates hunger

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. An increasingly common disease, diabetes mellitus has been diagnosed in approximately 463 million adults and 1.1 million children and adolescents under 19 years of age worldwide. In Australia, almost 1.2 million people (~5% of the total population) had been diagnosed with diabetes mellitus. In the United States, 18 million adults and more than 200,000 children were diagnosed with this disease. It is estimated that up to 7 million more adults have the condition but have not been diagnosed. In addition, approximately 79 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 recognised 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. It is acquired, and lifestyle factors such as poor diet, inactivity, and the presence of pre-diabetes greatly increase a person’s risk. About 80 to 90 percent of people with type 2 diabetes are overweight or obese. 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 diabetic will eventually require insulin.Two of the early manifestations of diabetes are excessive urination and excessive thirst. They demonstrate how the out-of-control levels of glucose in the blood affect kidney function. The kidneys are responsible for filtering glucose from the blood. Excessive blood glucose draws water into the urine, and as a result the person eliminates an abnormally large quantity of sweet 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 eyes 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.Diabetes is diagnosed when lab tests reveal that blood glucose concentrations are higher than normal, a condition called hyperglycaemia. 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. 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.

Section Review

The pancreas has both exocrine and endocrine functions. The pancreatic islet cell types include alpha cells, which produce glucagon; beta cells, which produce insulin; delta cells, which produce somatostatin; gamma cell which produce pancreatic polypeptide and epsilon cells which produce ghrelin. 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 utilisation 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 characterised 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.

Review Questions

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14.10 Organs with Secondary Endocrine Functions
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