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Metabolism > Postprandial Glucose Metabolism - Pancreatic Function > Flashcards

Postprandial Glucose Metabolism - Pancreatic Function Flashcards

1
Q

What is the endocrine role of the pancreas?

A

1-2% of weight in Islets of Langerhans; production and secretion of insulin, amylin, glucagon, somatostatin, and pancreatic polypeptide

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2
Q

What is the exocrine function of the pancreas?

A

98-99%; production and secretion of bicarbonate, amylase, trypsin, chymotrypsin, and carboxypeptidase for digestion

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3
Q

What is the structure of the pancreatic islets?

A

50-500um diameter sphere of 50-300 cells of 4 types: alpha, beta, delta, and theta; beta cells are 80% of the population and comprise the core; the other 3 comprise the outside

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4
Q

Beta cells secrete

A

(80%) insulin and amylin

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5
Q

Alpha cells secrete

A

(10%) glucagon

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6
Q

Delta cells secrete

A

(<5%) somatostatin

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7
Q

Theta cells secrete

A

(<5%) pancreatic polypeptide

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8
Q

Insulin is synthesized as a

A

preprohormone

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9
Q

Insulin is cleaved by

A

PC2 (pre) and PC1 (pro)

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10
Q

The cleaved segment of insulin gene is

A

C-peptide (connecting peptide)

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11
Q

Insulin forms from

A

disulphide bonds between the alpha and beta chains of the insulin gene with C-peptide cleaved from between them

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12
Q

Insulin is packaged into

A

secratory granules containing endopeptidase enzymes

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13
Q

Secretion of insulin is stimulated by

A

nutrients eg glucose

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14
Q

What are the 2 phases of insulin secretion?

A

sharp rise (2-5mins) of surface quick-released vesicles; prolonged secretion (for duration of stimulus)

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15
Q

How is the insulin release profile altered in type 2 diabetes?

A

1st/rapid phase of insulin secretion disappears

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16
Q

Which GLUT receptor takes up glucose into beta cells?

A

GLUT2

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17
Q

What is unique about GLUT2 and glucokinase?

A

They both have high Kms; they increase in proportion to the concentration of sugar present

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18
Q

How are beta cells signalled to secrete insulin?

A

Glucose enters cell via GLUT2; phosphorylated to G6P by glucokinase; enters glycolysis & TCA; increases ATP/ADP ratio which closes a K+ channel; causes depolarization of the membrane and opening of a Ca2+ channel; Ca2+ influx signals vesicle release

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19
Q

GLUT2 and glucokinase are only expressed in

A

beta cells and liver

20
Q

How do amino acids trigger insulin secretion by beta cells?

A

taken up by specific AA transporters; enter TCA as does G6P to increase ADP/ATP ratio, triggering membrane depolarization, Ca2+ influx, and vesicle release (like glucose does)

21
Q

How do fatty acids trigger insulin secretion by beta cells?

A

burning of FAs results in an increase in malonyl-CoA which inhibits entry of fats into mitochondria via the carnatine transporter for beta-oxidation; somehow this causes insulin secretion; also a FA receptor FFA1R

22
Q

more insulin is secreted when glucose is administered _______ than when administered ________

A

orally; intravenously - this phenomenon is called the incretin effect and is explained by the presence of incretin hormones from the gut causing insulin secretion

23
Q

What are incretins?

A

gut derived hormones that are secreted in response to nutrients (glucose, FAs, AAs) that increase insulin production

24
Q

What are the incretins?

A

glucagon-like peptide 1 (GLP-1) and glucose-induced insulinotropic polypeptide (GIP)

25
Q

GIP comes from the

A

upper small bowel

26
Q

GLP-1 comes from the

A

lower small bowel

27
Q

GLP-1 is a fragment of the

A

glucagon gene - processed to different hormones depending on tissue

28
Q

GLP-1 stimulates insulin secretion only when

A

glucose is high

29
Q

GLP-1 is secreted from

A

L-cells in small intestine in response to glucose and FA

30
Q

GLP-1 binds to

A

receptor on beta cells

31
Q

What are the actions of GLP-1?

A

stimulates insulin release and proinsulin/insulin biosynthesis (only if glucose is low); inhibits gastric emptying; inhibits glucagon secretion; promotes beta cell proliferation, differentiation, and maturation

32
Q

Why can’t GLP-1 be used directly in treatment of T2D?

A

half-life is only 2-3mins

33
Q

What are the incretin-based therapies?

A

DPP-4 inhibitors - incretin enhancers that inhibit the enzyme that degrades GLP-1; GLP-1R agonists -incretin mimetics eg exenatide

34
Q

What is exenatide?

A

byetta - GLP-1R agonist in the tx of T2D; causes a drop in HbA1c and some weight loss

35
Q

What is the concern over incretin-based therapies?

A

DPP-4 inhibitors and GLP-1R agonists may cause increases in pancreatitis and pancreatic cancer

36
Q

GIP is secreted from

A

K cells of duodenum in response to glucose and FAs

37
Q

What are the actions of GIP?

A

stimulates insulin release; activates lipoprotein lipase to enhance fat clearance from the blood; its effects are dependent on plasma glucose concentration

38
Q

GIP binds to

A

a receptor on beta cells

39
Q

Amylin is released from

A

beta cells

40
Q

What are the actions of amylin?

A

inhibits glucagon secretion; delays gastric emptying; inhibits food intake

41
Q

In type 1 diabetes, amylin

A

is deficient because the beta cells are destroyed

42
Q

Glucagon is secreted from

A

alpha cells in response to low blood glucose

43
Q

What is the action of glucagon?

A

stimulates liver to release glucose to restore normal blood glucose

44
Q

Pancreatic polypeptide is secreted from

A

theta cells after a meal

45
Q

What are the actions of pancreatic polypeptide?

A

inhibits food intake; increases energy expenditure; inhibits secretion of pancreatic enzymes; blocks contraction of gallbladder

46
Q

Somatostatin is released from

A

delta cells following a mixed meal

47
Q

What are the actions of somatostatin?

A

inhibits insulin and glucagon secretion; inhibits pancreatic exocrine function; main function to prevent exaggerated hormonal responses to a meal

Metabolism (16 decks)

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