test 7

Question 1

Major pancreatic hormones

Answer 1

• insulin and glucagon

* Secretion determined by plasma substrate levels

Question 2

What do insulin and glucagon do

Answer 2

• They coordinate disposition of nutrients from meals and the flow of endogenous substrates during fasting via actions on liver, adipose tissue, and muscle.

Question 3

Insulin

Answer 3

• The hormone of “abundance”. When nutrients are in excess, insulin stores the excess as fuel.

Question 4

Glucagon

Answer 4

• The hormone of “starvation” and promotes the mobilization these fuels when nutrient supply is low.

Question 5

endocrine cells of the pancreas

Answer 5

• The endocrine cells of the pancreas are arranged in clusters, called the ISLETS, which compose of 1-2% of the pancreatic mass
• Each cell contain 4 cell types
• The intimate contact of the cell types indicate a paracrine function; one cell type can alter the function or secretion of another nearby or adjacent cell type.

Question 6

Alpha cells secrete

Answer 6

• glucose

- 20% of islets cells

Question 7

Beta cells secrete

Answer 7

• insulin

- 65% of islets cells

Question 8

Delta cells secrete

Answer 8

• somatostatin

- 10% of islets cells

Question 9

F cells secrete

Answer 9

• pancreatic polypeptide

- 5% of islets cells

Question 10

Stimulants (secretagogues) of insulin release include:

Answer 10

• glucose
• amino acids (leucine, arginine)
• glucagon-like polypeptide (GLP-1)
• glucose-dependent insulinotropic polypeptide (GIP)
• glucagon
• cholecystokinin
• vagal activity

Question 11

Mechanism of insulin secretion by glucose

Answer 11

 Uptake of glucose into the Beta cell by a “glucose sensor”, GLUT2.
 Metabolism of glucose produces ATP.
 ATP closes the ATP-sensitive K+ channels, which depolarizes the -cell membrane.
 This opens the Ca2+ channels, allowing Ca2+ to flow inside, increasing [Ca2+]i.
 Increased Ca2+ causes exocytosis of insulin-containing granules.

Question 12

Disposal of glucose by insulin in peripheral tissues

Answer 12

 Insulin binds to an insulin receptor located in tissues; liver, muscle, adipose tissue.
 The insulin receptor is activated, and proteins of the insulin-receptor substrate (IRS) family are phosphorylated.
 The IRSs activate other kinases within the cell, which translates the insulin signal to metabolic effects; glucose and K+ uptake, glycogen synthesis, lipogenesis, cell growth.

Question 13

When your levels of sugar (glucose) go over your normal (>110 mg/dl)

Answer 13

• Insulin is released (Beta cells are activated):
  - activates glucose uptake
  - increases the use of glucose and ATP generation
  - converts glucose to glyocgen
  - increases amino acid absorption and protein synthesis
  - increases triglyceride synthesis (increases adipose tissue mass)
• all of this ultimately results in a decrease in glucose (blood sugar)

Question 14

When your levels of sugar (glucose) go below your normal (<70 mg/dl)

Answer 14

• glucagon is released (from Alpha cells)
  - increased breakdown of glycogen to glucose (in the liver and skeletal muscles)
  - increased breakdown of fats to fatty acids (adipose tissue)
  - increased synthesis and release of glucose (liver)

Question 15

Incretin (coming from the gut) effect

Answer 15

• the existence of gut-derived factors or hormones that enhance glucose-stimulated insulin secretion by the pancreatic β-cell
• Insulin secretion elicited by oral glucose is greater than following intravenous delivery.
• The incretins are glucose dependent insulinotropic peptide (GIP), and glucagon like peptide (GLP-1).

Question 16

As the food passes through the GI tract, what is being released and activated in the circulation

Answer 16

• glucose dependent insulinotropic peptide (GIP), and glucagon like peptide (GLP-1).

Question 17

glucose dependent insulinotropic peptide (GIP), and glucagon like peptide (GLP-1) target what and cause

Answer 17

• targets the Beta cell in the pancreas

- causes an increase in insulin production => increasing cellular glucose uptake

Question 18

glucagon like peptide (GLP-1) targets what and cause

Answer 18

• targets Alpha cells in the pancreas
• suppresses glucagon release
• which targets the liver
• decrease production of glucose => decrease in hepatic glucose output

Question 19

glucose dependent insulinotropic peptide (GIP), and glucagon like peptide (GLP-1) metabolized very quickly in the plasma by

Answer 19

• enzyme known as Dipeptidyl peptidase (DPP)

Question 20

Diabetes

Answer 20

• metabolic condition where blood sugar levels are extremely high

Question 21

Classification of diabetes: 4 classes

Answer 21

Type 1
Type 2
Type 3 ? (Associated with Alzheimer’s Disease)
Gestational
Other

Question 22

Type 1

Answer 22

• pancreas failure
• causes blood sugar to rise
  • Commonly affects children, adolescents, or young adults.
  • Characterized by insulin deficiency due to destruction of β-cells.
  • Loss of function results from autoimmune processes. Presence of islet cell antibodies or autoantibodies to insulin.
  • Pancreas fails to produce insulin and respond to glucose, and patients show classic symptoms of insulin deficiency (polydipsia (excessive thirst), polyphagia (excessive hunger), polyuria (sugar in urine), and weight loss).
  • Treatment requires exogenous INSULIN to control glucose and prevent ketoacidosis.

Question 23

Type 2

Answer 23

• Type 2 diabetes accounts for greater than 90% of cases.
• Etiology is unknown, but is influenced by genetic factors, obesity, ageing, physical inactivity.
• Type 2 ranges from insulin resistance (hyperinsulinemia) to insulin secretory defect with peripheral insulin resistance. Pancreas retains some β-cell function, but insulin secretion is inadequate.
• Blunted/decreased phase 1 and 2 insulin secretion.

Question 24

Insulin resistance

Answer 24

• Resistance is a lack of sensitivity of target organs to insulin.
• Weight loss, exercise, and diet modification decrease insulin resistance and improve glycemic control in some patients.
• However, most require some form of pharmacological intervention.