All Access Pass - 3 FREE Months!
Institutional email required, no credit card necessary.
Endocrine Pancreas

Endocrine Pancreas

Start 3-Month Free Access!
No institutional email? Start your 1 week free trial, now!
Pancreatic endocrine cells
  • Comprise the Islets of Langerhans: each of which is a cluster of 4 endocrine cell types, whose products are ultimately secreted into the hepatic portal blood and delivered to the liver.
  • A key function of pancreatic endocrine cells is to maintain basal blood glucose concentration via regulated storage and release: glucose is a major source of energy for the body.
  • In order to maintain homeostatic blood glucose concentrations, the islet cells engage in communication via neural, hormonal, and cell-to-cell signaling.
Pancreatic endocrine cell types:
Alpha cells
  • Comprise approximately 20% of the islet cells
  • They secrete glucagon, which increases blood glucose concentrations between meals.
Beta cells
  • Comprise approximately 65% of the islet cells
  • They secrete insulin, which lowers blood glucose concentrations after a meal.
Delta cells
  • Comprise approximately 10% of the islet cells
  • Secrete somatostatin, which inhibits insulin and glucagon secretion to moderate their effects on blood glucose concentrations.
F cells
  • Are rare
  • They secrete pancreatic polypeptides, whose specific functions are uncertain.
Beta cell insulin secretion.
  • Beta cells release insulin in response to multiple stimuli, but glucose is the primary stimulus.
Step 1:
  • Glucose diffuses into the beta cell via GLUT – 2 receptors;
Step 2:
  • Within the cell, glucose is phosphorylated by the enzyme glucokinase.
Step 3:
  • Oxidation of phosphorylated glucose produces ATP.
Step 4:
  • ATP closes potassium channels, trapping potassium inside the cell.
  • This depolarizes the cell membrane.
Step 5:
  • In response to depolarization, calcium channels open, and the intracellular calcium concentration increases.
Step 6:
  • This triggers exocytosis of insulin-containing vesicles.
Bear in mind that the beta cell response to fatty acids and proteins is similar, though not identical.
As discussed in detail elsewhere, insulin is released into the nearby capillaries, drains into the hepatic portal system, and, eventually, enters systemic circulation to reach its target tissues.
Clinical Correlations:
Insulin-dependent, aka, Type I diabetes
  • Destruction of beta cells (often by autoimmune disorders) causes insufficient circulating levels insulin; thus, carbohydrate, protein, and fat metabolism is inhibited.
  • Because Type I diabetes is due to insulin insufficiency, insulin replacement therapy is the primary treatment to normalize blood nutrient concentrations.
Insulin-resistant, aka, Type II diabetes
  • Down-regulation of insulin receptors on target tissues, specifically in the liver, skeletal, and adipose tissues, inhibits metabolism of carbohydrates, protein, and fat.
  • Despite normal, or even elevated, levels of insulin, the target tissues cannot respond as usual; thus, treatment includes insulin receptor sensitizers (in addition to insulin therapy).

Related Tutorials