Insulin and Glucagon Flashcards

1
Q

how long would plasma glucose last? glycogen? fat?

A

1 hour
part of one day
40 days with water

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2
Q

how much protein is in the body and how much of it could be use for energy needs?

A

10-12 kg

1/2 is available

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3
Q

what is the normal blood concentration of glucose?

A

80-100 gm/dL

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4
Q

what is the role of somatostatin in the pancreas?

A

prevents release of insulin and glucagon

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5
Q

what is the brain energy source? how much oxygen does it require?

A

glucose

20% of resting oxygen supply

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6
Q

what are the three types of islets of langerhans cells and what do they secrete?

A

alpha- glucagon
beta- insulin
delta- somatostatin

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7
Q

where is pancreatic polypeptide secreted? what does it do?

A

GI hormone synthesized by F cells at the periphery of the islet (with alpha and delta cells)
inhibits gallbladder contraction and pancreatic exocrine secretion

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8
Q

when is pancreatic polypeptide secreted?

A

during strenuous exercise, after ingestion of a protein rich meal or during hypoglycemia

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9
Q

how is glucagon synthesized?

A

it is translated as pre-proglucagon and processed postranslationally into glucagon, glicentin, GLP-1 and 2 and glicentin- like peptide
stored in membrane bound granules

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10
Q

what happens to glucagon after it is released?

A

it is degraded by the liver and kidney (not excreted)

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11
Q

what are stimulators of glucagon secretion?

A

hypoglycemia <50mg/dl
increase in arginine and alanine (protein degredation)
exercise and stress

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12
Q

what are three inhibitors of glucagon secretion?

A

insulin, somatostatin and hyperglycemia

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13
Q

what are the counter regulatory hormones? what do they do?

A

glucagon, catecholamines, growth hormone and cortisol

keep blood glucose high enough for brain

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14
Q

what is the primary target of glucagon? what does it do?

A

liver

increases blood glucose- glycogenolysis, gluconeogenesis, and lypolysis

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15
Q

what does glucagon do in adipose tissue?

A

decreases glycolysis and promotes release of fatty acids

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16
Q

how is insulin synthesized?

A

synthesized in perproinsulin form

processed in storage granules with endopeptidase (secreted together)- cleaved into insulin and C peptide

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17
Q

why is zinc included in secretory granules?

A

to join 6 insulin molecules into hexamers

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18
Q

what are levels of C peptide used for?

A

to quantitate endogenous insulin production when patients receive insulin injections

19
Q

what type of insulin is used to inject to diabetic patients?

A

crystalline zinc insulin

20
Q

how is insulin degraded?

A

insulinases in liver, kidney and other tissues

21
Q

describe postprandial insulin secretion.

A

there is an early phase of insulin release after 10 min and a peak at 30-45 min (late phase)

22
Q

describe release of insulin with IV glucose.

A
early phase (release of stored insulin) which falls in 10 min
late phase if stimulus is maintained- reflects newly formed
23
Q

what is the mechanism of insulin secretion from beta cells?

A

1 GLUT 2 transporter mediates diffusion of glucose in
2 increase in ATP due to glucose metabolism
3 ATP inhibits a K channel-cell voltage increase
4 depolarization activates Ca channel and Ca induced Ca release
5 elevated Ca leads to fusion of vesicles- insulin release

24
Q

besides glucose, what else can modulate insulin secretion?

A

amino acids, other monosaccharides, and certain hormones

25
Q

describe the phases of digestion with respect to insulin.

A

cephalic phase- vagus mediates small rise in insulin

intestinal phase- glucose absorption stimulates secretion

26
Q

what do incretins do?

A

provide advance notice of feeding and stimulate insulin secretion
CCK, GIP and GLP-1 increase insulin during feeding

27
Q

describe the effects of epinephrine and NE on beta cells.

A

epinephrine- stimulates secretion (beta receptor)

NE- supresses insulin (alpha receptor)- from postsynaptic nerve terminals

28
Q

what is the net effect of sympathetic action on beta cells?

A

there is a net supression of insulin secretion

29
Q

what is insulin’s effect on the liver?

A

stimulates glucose uptake, glycogenesis, lipogenesis, glycolysis and protein synthesis

30
Q

what is insulin’s effect on myocytes?

A

stimulates glucose uptake with increase GLUT 4 on surface, promotes glycogenesis and glycolysis
also stimulates lipogenesis and protein synthesis (AA uptake also)

31
Q

what is insulin’s effect on adipocytes?

A

increase in GLUT 4 and LPL export to capillaries. also increases glycolysis and esterification of fats

32
Q

what is the difference in results of a glucose tolerance test with diabetes?

A

plasma glucose will rise higher and remain there longer

33
Q

what disease causes insulin deficiency? insulinemia? glucagon deficiency?

A

type 1 diabetes
insulin shots and insulinoma
glucagon deficiency very rare

34
Q

what are orixigenic factors? give an example

A

neurotransmitters that stimulate feeding

neuropeptide Y

35
Q

what are anorexigenic factors? give 4 examples

A

neurotransmitters that inhibit feeding

GLP-1, corticotropin releasing hormone, alpha MSH and CART

36
Q

what do satiation sinals do?

A

secreted in response to food ingestion, act within timeframe of single meal and reduce meal size

37
Q

where is the primary control of food intake?

A

hypothalamus

38
Q

which GI peptides reduce meal size?

A

CCK, GLP-1, GLP-2, glucagon, and PYY

39
Q

what pathway carries information that fat and protein has been eaten?

A

nucleus of the solitary tract

40
Q

where is ghrelin secreted and what does it do?

A

secreted from oxyntic glands of stomach

stimulates food intake by acting on arguate nucleus to increase NPY and inhibit CART

41
Q

what hormones are secreted in proportion to the amount of fat in the body?

A

leptin and insulin- enter hypothalamus to influence energy homeostasis

42
Q

what contributes to meal onset signals and what do they activate?

A

environmental factors, low leptin, hypoglycemia, hypoinsulinemia and negative energy balance
activate orexin and MCH expression

43
Q

what strategies need to be devised for long term weight loss success?

A

counteracting hormonal changes to weight loss that stimulate appetite