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Drew 921 > 6_InsulinGlucagon > Flashcards

6_InsulinGlucagon Flashcards

1
Q

Who discovered insulin in 1923?

A

Frederick Banting and John Macleod

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2
Q

Who sequenced insulin in 1958?

A

Fredrick Sanger

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3
Q

Who performed x-ray crystallography of insulin in 1964?

A

Dorothy Hodgkin

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4
Q

Who developed RIA to measure insulin concentration?

A

Rosalyn Yellow

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5
Q

What structures make up the exocrine glands of the pancreas?

A

acini

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6
Q

What structures make up the endocrine glands of the pancreas?

A

islets of langerhans

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7
Q

Function of the alpha cells?

A

secrete glucagon

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8
Q

Function of the delta cells?

A

secrete somatostatin

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9
Q

Function of the beta cells?

A

secrete insulin, C peptide, and amylin

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10
Q

Function of the PP cell?

A

secretes pancreatic polypeptide

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11
Q

What are the pancreatic cells’ relative percentages of abundance of the pancreas?

A

alpha = 25%, beta = 60%, delta = 10%

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12
Q

How is insulin stored?

A

in secretory granules as the hexamer

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13
Q

Describe insulin’s half-life and binding in plasma?

A

unbound, 6 minutes

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14
Q

Describe the structure of insulin.

A

A and B chains linked by 2 di-sulfide bridges; A chain has third disulfide bridge

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15
Q

How many AA’s is insulin, and what is its mass?

A

51 AA, 5.8 kDa

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16
Q

What kind of receptor is the insulin receptor?

A

RATK

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17
Q

What factors cause an increase in insulin secretion?

A

1) glucose, 2) glucagon, 3) GH, 4) cortisol, 5) FFAs, 6) Arg/Lys, 7) GI hormones, 8) PNS, 9) beta-adrenergic stimulation, 10) insulin resistance/obesity

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18
Q

What are the mechanisms of the sulfonylureas?

A

ATP-gated K+ channel blockers prevent depolarization of the beta cell

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19
Q

What factors cause a decrease in insulin secretion?

A

decrease in glucose, fasting, somatostatin, alpha-adrenergic stimulation, leptin

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20
Q

Describe the events leading up to insulin secretion.

A

1) GLUT2 imports glucose causing increase in ATP, 2) ATP closes ATP-gated K channel causing depolarization, 3) Ca channels are activated 4) Ca stimulates vesicle-plasmalemma fusion causing exocytosis

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21
Q

How many phases in insulin secretion?

A

Phase I and Phase II

22
Q

Describe Phase I of insulin release.

A

initial release of stored insulin within 3-5 minutes

23
Q

Describe Phase II of insulin release.

A

release of additional stored insulin and new synthesis at 15 minutes; peaks at 2-3 hours

24
Q

What is proinsulin?

A

A, B, and C peptides of insulin still joined

25
Q

When is proinsulin cleaved?

A

in the secretory granule

26
Q

What is the initial translation product of the insulin mRNA?

A

pre-proinsulin

27
Q

Describe the structure of the insulin RATK.

A

2 extracellular alpha chains disufide-bonded to 2 membrane-spanning beta chains

28
Q

Describe the receptor pathway for the InsRATK

A

glucose binds the alpha subunits; beta subunits are auto-phosphorylated; local TK activated

29
Q

When do muscle cells become more permeable to glucose for glucose utilization?

A

with insulin secretion and during contraction

30
Q

What is the normal energy source of muscle cells?

A

fatty acids; only slightly permeable to glucose without insulin

31
Q

What is the function of the SREBP-1c gene?

A

produces a transcription for an increase in FA synthesis enzymes

32
Q

Where kind of glucose receptors does the liver have?

A

GLUT-1

33
Q

How does GLUT-1 respond to insulin?

A

it doesn’t

34
Q

What are insulin’s effects in the liver?

A

1) increased FA synthesis from glucose if glycogen at its 5-6% capacity via upregulation of SREBP-1c; 2) increase uptake & storage of glucose by activating glycogen synthesis enzymes; 3) decreases glycogenolysis by inactivating liver phosphorylase and glucose phosphatase; 4) decreases gluconeogenesis

35
Q

What causes gluconeogenesis and glucose release from the liver under fasting conditions?

A

lack of insulin (just takes off the brakes)

36
Q

What is the rate-limiting step in FA synthesis?

A

acetyl-CoA-carboxylase (acetyl-CoA to malonyl-CoA)

37
Q

What are insulin’s effects in adipocytes?

A

1) primarily inhibits hormone-sensitive lipase to decrease stored TG hydrolysis; 2) promotes GLUT4 translocation for TG synthesis; 3) increases FA synthesis; 4) increases G3P synthesis

38
Q

How are FFAs created in adipose tissue?

A

from FFA’s in blood, from stored TG hydrolysis, and from de novo synthesis

39
Q

What are insulin’s effects of protein metabolism?

A

1) increased anabolism, 2) decreased gluconeogenesis, 3) increased AA uptake (synergistic with GH)

40
Q

What are insulin’s effects in the brain?

A

none; insulin not required for glucose uptake

41
Q

What happens in insulin lack?

A

HPL activated to increase FFA’s; ketone bodies increase

42
Q

What are the effects of somatostatin?

A

extends time for nutrient absorption: 1) decreases insulin, 2) decreases glucagon, 3) decreases GI motility, 4) decreases GI secretions and absorption

43
Q

What is the half-life of somatostatin?

A

3 minutes

44
Q

How is glucagon synthesized?

A

as a pre-prohormone

45
Q

Describe glucanon’s binding and half-life.

A

short half-life, unbound

46
Q

What is glucagon’s receptor pathway?

A

1) primary is G-alpha-S to activate PKA; 2) minor pathway is G-alpha-q; 3) also decreases glycogen synthase

47
Q

What are PKA’s effects when stimulated by glucagon?

A

1) glycogenolysis (activates GPK); 2) gluconeogenesis (activates PGC1, PEPCK, G6P)

48
Q

What enzymes does glucagon activate?

A

G6Pase, GPK

49
Q

What enzymes does glucagon inhibit?

A

Glycogen synthase

50
Q

How is glucagon secretion stimulated?

A

1) hypoglycemia, 2) exercise, 3) increased Ala/Arg

51
Q

Why do increased Ala and Arg stimulate glucagon release?

A

glucagon facilitates AA conversion to glucose

52
Q

What effect do increased Ala/Arg have on insulin secretion?

A

stimulate! Same as glucagon.

Drew 921 (33 decks)

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