Endocrine Pancreas

Question 1

What is the primary type of cell in the Islet of Langerhans? What do they produce?

Answer 1

Beta cells (insulin)

Question 2

What types of cells lie on the mantle/outer edge of the Islets of Langerhans? What do they produce?

Answer 2

alpha cells (glucagon), S cells (somatostatin), F or PP cells (pancreatic polypeptide)

Question 3

Where in the islet does oxygenated blood travel first?

Answer 3

To the beta cells in the middle, so arterioles receive the densest concentration of insulin. Insulin can thus have affect on alpha cells as it leaves the islet and affect glucagon release

Question 4

Which chain of insulin is the active chain?

Answer 4

B chain

Question 5

What two products will proindulin break into?

Answer 5

C peptide + insulin

Question 6

When trying to determine how much insulin a person makes endogenously, what do you measure and why

Answer 6

C peptide b/c has a longer half life than insulin - also when we take someone’s blood, it won’t be an accurate measure of insulin b/c organs like the liver use up a bunch of insulin

Question 7

What increases secretion of insulin?

Answer 7

Glucose, glucagon, GLP-1, beta-adrenergic activity

Sulfonylureas, K+, Ca2+, GIP, CCK

Question 8

What decreases secretion of insulin?

Answer 8

Fasting, excercise, somatostatin, alpha-adrenergic activity

IL-1, prostaglandin e2

Question 9

Describe process of GSIS (glucose-stimulated insulin secretion)

Answer 9

1. Glucose enters through GLUT2
2. Goes through glycolysis and makes ATP
3. ATP blocks ATP-dependent K+ channels that leak K+ so cell depolarizes
4. voltage-gated Ca channels open and influx of Ca allows for further depolarization
5. Preformed insulin vesicles fuse to membrane for release

Question 10

What is responsible for immediate spike in insulin levels prior to gradual increase of insulin levels right after eating?

Answer 10

Incretin - GLP1 and GIP - they are synthesized by L cells of duodenum after stimulation by vagus nerve to prevent hyperglycemia right after eating

Question 11

What are effects of insulin on carbohydrate metabolism in liver, muscle, and adipose tissue?

Answer 11

Liver - breaks down glucose for energy if needed, makes glycogen, cholesterol and fat
Muscle - stimulates glucose uptake, then oxidizes or stores it (storage mostly)
Adipose - stimulates glucose uptake - triglyceride formation and storage

Question 12

What are effects of insulin on fat metabolism in liver, muscle, and adipose tissue?

Answer 12

Liver - Increase fat synthesis and TAG synthesis for export as VLDLs
Muscle - Inhibit muscle lipoprotein lipase and FFA uptake and oxidation
Adipose - Inhibits HSL, stimulates adipose lipoprotein lipase to increase FFA availability to fat cells (lipogenic + anti-lipolytic because anti-ketogenic)

Question 13

What are effects of insulin on protein metabolism?

Answer 13

Anabolic - increases AA uptake and protein synthesis

Anti-catabolic - decreases proteolysis

Question 14

What is diabetic ketoacidosis result of?

Answer 14

Result of very low levels of insulin leading to lots of plasma FFAs as insulin normally causes lipogenesis and stores FFA as fat

Body becomes hyperglycemic, but glucose cannot be taken into cells b/c of low insulin levels, so body tries to use fats - eventually you run out of glucogenic precursors to oxidize the fats and ketone bodies are produced instead

Question 15

Where is somatostatin produced? (two places)

Answer 15

Hypothalamus and pancreatic islets

Question 16

What is effect of somatostatin on pituitary gland?

Answer 16

Inhibit GH

Question 17

What is effect of somatostatin on pancreas and GI system?

Answer 17

Inhibits all endocrine and exocrine secretions including HCl, pepsin, gastrin, secretin, glucagon and insulin, SI juices