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U6 Physiology > Insulin & Glucagon - CB > Flashcards

Insulin & Glucagon - CB Flashcards

1
Q

What do beta cells produce?

A

insulin

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2
Q

What do alpha cells produce?

A

glucagon

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3
Q

What do delta cells produce?

A

somatostatin

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4
Q

What do F cells produce?

A

Pancreastic polypeptide

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5
Q

What does pancreatic polypeptide do?

A

inhibits gallbladder contractions and pancreatic enzyme secretions

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6
Q

what does glucagon do?

A

a catabolic hormone. mobilizes energy stores

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7
Q

What does insulin do?

A

anabolic activities, energy storage

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8
Q

What does somatostatin do?

A

inhibits insulin,glucagon, gastrin, all gut hormones, and gastric acid release

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9
Q

Describe glucagons post translational processing. Where is it degraded?

A

160 AA pre-proglucagon → glucagon + glicentin, glicentin-like peptide, GLP1 and GLP2

liver (80%) and kidneys

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10
Q

What stimulates glucagon secretion?

A

hypoglycemia, increase in arginine and alanine (indicative of protein degradation), exercise, stress

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11
Q

What inhibits glucagon secretion?

A
  1. somatostatin
  2. insulin
  3. hyperglycemia
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12
Q

What is the primary target organ of glucagon? What proceses does it trigger?

A

Liver

Glycogen lysis, gluconeogen., liplysis

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13
Q

What effect does glucagon have in adipose tissue?

A

decreased glycolysis, increased lipoysis

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14
Q

Describe the processing of proinsulin?

A
  1. insulin synthesized in preproinsulin form, packed into Golgi and then into granules along with endopeptidase with trypsin-like activity → proinsulin and endopeptidase are secreted together. secretory granules contain Zn, which joins insulin molecules into hexamers
  2. proinsulin cleaved into → insulin and C peptide
    - C peptide no known biological activity, but used to quantitate endogenous insulin production in patients receiving exogenous insulin
    - crystalline Zn-insulin is basic preparation used to treat diabetes mellitus
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15
Q

What is the half life of insulin? where is it degraded?

A

insulin half life ~5-8 minutes and degraded by insulinase in liver, kidney, other tissues

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16
Q

How is insulin secretion regulated?

A

glucose stimulates the release, mediated by calcium influx

  1. fast component/early stage of insulin release occurs ~10 minutes of food ingestion, peaks at ~30-45 minutes
    - first peak of insulin is likely release of stored insulin
  2. fast component falls within 10 minutes
    - if stimulus for insulin secretion maintained, release increases gradually during next hour
    - later rise in insulin = late phase, likely due to release of newly formed insulin
17
Q

decribe the phasic response of insulin after feeding.

A
  1. incretins give advance notice of feeding and stimulate insulin secretion
    - oral glucose yields more insulin than does IV glucose due to prediction of rise
    - CCK and GIP both enhance insulin secretion
    - GLP1 similarly increases insulin during feeding
  2. Cephalic phase – gastric acid secretion and small rise in plasma insulin mediated by vagus nerve
  3. intestinal phase – increased glucose from absorption = primary stimulus for insulin secretion
18
Q

What affect does epinephrine binding to beta adrenergic cells have on insulin?

A

stimulates secretion

19
Q

What affect does norepinephrine binding to alpha adrenergic cells have on insulin?

A

inhibits secretion (this mechanism prodominates) prevents hypoglycemia during excercise

20
Q

What effects does insulin have in the liver?

A

promotes: glycogen syn, glycolysis, lipogenesis, protein syn
inhibits: glycogenlysis, fat oxidation, gluconeogen., ketogenesis, protein breakdown

21
Q

What effects does insulin have in the muscle?

A

glucose uptake by GLUT4, promotes glycogenesis, glycolysis, lipgenesis, protein syn
inhibits: protein degradation

22
Q

What effects does insulin have in the adipocytes?

A

insulin stimulates glucose uptake via GLU4

  1. also increases glycolysis, producing a-glycerophosphate in turn increasing esterification of fats
  2. stimulates synthesis of LPL which moves to surface of endothelium and releases fatty acids from chylomicrons and VLDL
23
Q

What are orexigenic factors?

A

neurotransmitters like NPY increasing feeding

24
Q

What are anorexigenic factors>

A

neurotransmitters inhibiting feeding like CRH (corticol tropin releasing hormone), GLP1 (glucagon like peptide), a-MSH (alpha-melanocyte stimulating hormone), cocaine-and-amphetamine related transcript (CART)

25
Q

What are satiation signal?

A

increase in response to food ingestion, reduce meal size, CCK, GLP1, PYY

26
Q

What is cholecystokinin? What cells release it?

A

satiation signal, made in I cells, binds to the vagal sensory system

27
Q

What is Ghrelin?

A

Ghrelin secreted from oxyntic glands of stomach and is only GI hormone that stimulates food intake

increase before meals and decreases after meals, working directly on ARC to enhance NPY/AgRP and inhibit POMC/CART

28
Q

What stimulates POMC? what does POMC produce

A

insulin and leptin, POMC produces alpha MSH (anorexigenic)

29
Q

What inhibits AgRP and NPY and stimulates POMC (alpha MSH)

A

Insulin and leptin

30
Q

What does a leptin and leptin receptor mutation cause?

A

Obesity

31
Q

What does the MC4R receptor (ligand is alpha MSH) mutation cause?

A

obesity

U6 Physiology (13 decks)

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