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Endocrine > Insulin and Glucagon > Flashcards

Insulin and Glucagon Flashcards

1
Q

The absorptive phase of substrate metabolism

A

Absorptive: during a meal blood levels of glucose, fatty acids, and amino acids increase allowing increased glycolysis and synthesis (FAO, Catabolic processes are inhibited)

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2
Q

Carbohydrates from meal

A

glycolysis increases, glycogen storage in muscles, fatty acid long chains in liver for storage

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3
Q

Citrate and Acetyl CoA

A

are both activated during glycolysis, Citrate activated fatty acid synthesis

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4
Q

Citrate mechanism

A

converts acetyl-CoA into malonyl-CoA which inhibits CPT1

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5
Q

Amino acids in absorptive phase

A

stimulated to enter cells for repair and replacement; excess are converted to TAG in liver

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6
Q

Fatty acids in absorptive phase

A

Fatty acids –>(liver) TAG—> (mobilized) in blood –> capillary walls (LIPOPROTEIN LIPASE) cleaves TAG to fatty acids for transfer into adipose cell–> fatty acid (in adipose cell) esterifies with glycerol to from TAG

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7
Q

Obligatory users of glucose

A

brain, RBC, nerves, intestinal mucosa, and renal medulla

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8
Q

Obligatory users of glucose have

A

highly sensitive glucose receptors and can utilize glucose even at low levels (>60)

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9
Q

CNA impairment is glucose drops below

A

60mg/100ml

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10
Q

Post-absorptive phase

A

goal to maintain plasma glucose through glycogenolysis, gluconeogenesis, lipolysis, and protein breakdown

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11
Q

Post-absorptive carbohydrates and protein

A

initially = glycogenolysis

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12
Q

Glucose-6-phosphate

A

enzyme that releases glucose into the bloodstream (muscle and brain do NOT have this)

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13
Q

muscle lacks G-6-P

A

converts glucose to lactate and secretes lactate which will go to the liver (Cori cycle) to be converted to glucose

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14
Q

After glycogenolysis, what occurs to maintain glucose levels

A

gluconeogenesis (lactate, pyruvate, glycerol, and AA)

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15
Q

Randle Effect

A

b-oxidation FAO can inhibit glycogenolysis to promote usage of fat as fuel

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16
Q

Transporting fatty acids into the mitochondria requires

A

acyl-CoA exchange of CoA for carnitine by CPT1

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17
Q

Once in the mitochondria acyl-carnitife is converted back to

A

acyl-CoA by CPT2

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18
Q

Ketogenesis

A

adaptation to starvation; during fasting mobilization of free fatty acids can be converted to ketones for alternative energy substrates for brain and other tissues; insulin ensures that ketone concentrations do not get too high

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19
Q

Type I DM

A

ketoacidosis can occur because of their lack of insulin to keep the ketones in balance during times of fasting

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20
Q

Pancreas

A

Alpha cells- glucagon
beta- insulin
D cells- somatostatin
F cells- pancreatic polypeptide

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21
Q

Insulin synthesis

A

preproinsulin formed in the beta cells of islets of langerhans cleaved into insulin and C-peptide and packaged in secretory vesicle

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22
Q

GLUT2

A

glucose receptor on beta cells

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23
Q

High plasma glucose

A

enters beta cells (GLUT2), increase in ATP, inhibit in K ion channels OPEN, depolarization, increase intracellular Ca, exocytosis of insulin

24
Q

Sulfonylureas

A

close K+ channels to cause depolarization and release of insulin

25
Q

Diazoxide

A

open K channels to hyperpolarize cell and inhibit insulin release

26
Q

adrenergic stimulation of alpha-2 receptors on beta cells

A

inhibits insulin secretion

27
Q

Insulin biphasic pattern

A

initial insulin spike (due to pre-synthesized hormone) followed by slower rise in insulin

28
Q

Glucose levels of _______ or less do not stimulate insulin

A

80

29
Q

The only time insulin and glucagon are stimulated simultaneously is

A

after a HIGH PROTEIN, no carb meal

30
Q

Somatostatin ________ insulin secretion

A

inhibits

31
Q

GI hormones ________ insulin secretion

A

promote

32
Q

Catecholamines (EPI and NE) ____________ insulin secretion

A

inhibit (this prevents hypoglycemia during exercise)

33
Q

Insulin binding causes

A

autophosphorylation of tyrosine kinase receptor, cAMP, IP3, and DAG responses that causes activation of anabolic processes and inhibition of catabolic

34
Q

Glucose-dependent tissues (brain, nerves, RBC, intestinal mucosa, and renal medulla)

A

glucose transporters independent of insulin and dependent on plasma glucose (Sensitive)

35
Q

GLUT4

A

glucose transporters on all other tissues that are insulin dependent

36
Q

IN adipose tissue insulin

A

increased lipoprotein lipase for the transfer of fatty acids into fat cell and increased fat synthesis

37
Q

Insulin __________ lipoprotein lipase in muscle

A

inhibits; divert fatty acids to adipose for storage not to muscle for usage

38
Q

Insulin’s effect on Na/K ATPase and K, PO, and Mg uptake

A

insulin causes uptake of K, PO, and Mg and ATP production for the cell to use these in synthesis of glycogen and protein

39
Q

Insulin directly _________ glucagon

A

inhibits; direction of blood flow goes from beta cells to alpha, therefore glucagon releasing cells are exposed to the highest level of insulin

40
Q

Metabolism of insulin

A

liver and kidney, half-life of 5-8 min

41
Q

Glucagon synthesis

A

pancreatic alpha cells, precursor molecule, Ca-dependent release

42
Q

Synaptotagmin-7 Ca-sensing protein

A

initiates the glucagon release

43
Q

Glucagon mechanism

A

cAMP 2nd messenger

44
Q

Glucagon mainly acts on

A

LIVER (only acts on uncle and fat when its VERY HIGH, such as in Type I DM)

45
Q

Glucagon effects

A

stimulation of glycogenolysis, gluconeogenesis, may stimulate lipolysis (@ HIGH conc), beta-oxidation, ketogenesis, AA gluconeogenesis, preoteolysis (@ HIGH conc)

46
Q

Stimuli that increase glucagon

A

low glucose, low fatty acids, high amino acids, high cortisol, catecholamines

47
Q

Stimuli that decrease glucagon

A

insulin, somatostatin, low AA, high glucose, and high fatty acids

48
Q

Metabolism of Glucagon

A

liver and kidney (same as insulin)

49
Q

Hormones that act/stimulate glucagon (counter-regulatory hormones to insulin)

A

catecholamines (EPI), cortisol, and GH (work under conditions of stress/exercise)

50
Q

First line of defense to hypoglycemia

A

decreased insulin, increased glucagon, and increased epinephrine

51
Q

Diabetes and insulin-dependent tissues

A

inability to uptake glucose stimulates gluconeogenesis adding to the hyperglycemia already experienced
inability to uptake AA, leading to proteolysis and elevates excretion of N and (-) Nitrogen balance

52
Q

Which diabetes (Type I or II) will have increased glucagon secretion?

A

Type 1: without insulin, glucagon will not be inhibited

53
Q

Why doesn’t ketoacidosis occur in Type II DM

A

because the presence of insulin limits lipolysis and ketone production

54
Q

CHronic acidosis as seen in ketoacidosis may lead to

A

HYPERKALEMIA: elevated plasma K because cells exchange/pick up H and release K which can lead to overall K DEFICIT as it is excreted

55
Q

Metabolic Syndrome

A

abdominal obesity, diabetes type II, elevated TAG, decreased HDL, elevated LDL, HTN,

56
Q

INsulin resistance

A

decreased receptors, decreased GLUT4 transporters, decreased intracellular mechanisms

57
Q

Treatment of Type II diabetes

A

SULFONYLUREAS: stimulate insuline release from beta cells OR exogenous insulin shots

Endocrine (9 decks)

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