L21: Endocrine+Pancreas Flashcards

1
Q

Islet of langerhans

A

endocrine cells in a sea of exocrine tissue (the rest of the pancreas)

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2
Q

beta cells produce

A

insulin, amylin

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3
Q

alpha cells produce

A

glucagon

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4
Q

delta cells produce

A

somatostatin (14 amino acid polypeptide hormone)

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5
Q

gamma cells produce

A

pancreatic polypeptide

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6
Q

epsilon cells produce

A

ghrelin

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7
Q

amylin

A

acts on the CNS to suppress appetite

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8
Q

somatostatin

A

inhibits digestive function

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9
Q

pancreatic polypeptide

A

putatively reduces appetite and food intake

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10
Q

ghrelin

A

appetite stimulating

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11
Q

Stimulate insulin secretion

A
  1. GI hormones (incretins)
  2. PNS
  3. Increased blood glucose and amino acid concentration
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12
Q

Inhibits insulin secretion

A

Epinephrine

Sympathetic stimulation: alpha-adrenergic

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13
Q

Cleaved off proinsulin during post-translational processing

A

C-peptide

a marker of insulin production/beta cell function

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14
Q

inside of secretory granule of insulin

A

Insulin
C peptide
small amounts of proinsulin

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15
Q

how does glucose enter beta cells?

A

GLUT-2

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16
Q

once inside beta cells, glucose

A

is phosphorylated to Glucose-6-phosphate (trapped)

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17
Q

Oxidation of glucose-6-phosphate yields

A

ATP

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18
Q

ATP in beta cells causes

A

K+ channel to close: decreased K+ flux: depolarization

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19
Q

depolarization of the beta cell membrane causes

A

voltage gated calcium channels to open

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20
Q

Trigger for exocytosis of insulin vesicles

A

increased intracellular calcium

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21
Q

effects of insulin on carbohydrates

A

decrease blood glucose

increase storage

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22
Q

effects of insulin on lipids

A

decreased blood fatty acids

increased storage

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23
Q

effects of insulin on proteins

A

decreased blood amino acids

increased storage

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24
Q

glucose is stored as

A

glycogen

triglycerides

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25
Q

amino acids are stored as

A

protein

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26
Q

GLUT1

A

transports glucose across blood brain barrier

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27
Q

GLUT2

A

transports glucose in kidney and intestines

28
Q

GLUT3

A

transports glucose into neurons

29
Q

GLUT4

A

insulin-dependent transporter in adipose tissue and resting muscle cells
insulin binds–>second messengers –> GLUT4 brought to surface of cell

30
Q

HbA1C value which reflects above average blood glucose over previous 3 months

A

> 6.5%

31
Q

glucosuria

A

glucose in urine since elevated glucose exceeds what tubular cells can reabsorb
causes osmotic diuresis

32
Q

Polyphagia

A

increased appetite due to decreased intracellular glucose

33
Q

Polydipsia

A

increased thirst

34
Q

ketone bodies cause metabolic acidosis, the body compensates by

A

Respiratory ventilation to blow CO2 off and bring pH back up

35
Q

lack of insulin shifts metabolism towards

A

more protein catabolism (muscle atrophy), amino acids in bloodstream

36
Q

excess blood amino acids cause

A

shift to gluconeogenesis in liver, making hyperglycemia worse

37
Q

2 ways by which hypoglycemia may occur

A
  1. Insulin overdose

2. Reactive hypoglycemia

38
Q

Reactive hypoglycemia

A

in extreme response to glucose, beta cells release too much insulin

39
Q

Reactive hypoglycemia shouldn’t be treated by

A

eating sugar, will worsen problem

40
Q

Glucagon is inhibited by

A
High glucose
Somatostatin
insulin
fatty acids
ketoacids
41
Q

Glucagon is stimulated by

A
*Low glucose*
Epinephrine (B2)
Vagal stimulation
CCK
fasting
exercise
increased dietary protein (arginine) in absence of carbs
42
Q

Glucagon

A

14 amino acid polypeptide

43
Q

a meal which is a combination of protein and carbs

A

has no effect on glucagon

44
Q

Glucagon is produced as

A

Proglucagon–> glucagon, incretin (GLP1)

45
Q

Incretin (GLP1)

A

released from intestine in response to high glucose in intestinal lumen
increases insulin release

46
Q

Glucagon effects

A

targets liver to stimulate hepatic glucose output

opposite of insulin

adipose tissue: pro-lipolytic effect

47
Q

Glucagon effects on carbohydrates and lipids

A

increased blood glucose, fatty acids, and ketones

48
Q

Glucagon effects on blood amino acids

A

minimal

hepatic protein degradation is used for gluconeogenesis, not to release amino acids to blood

no effect on skeletal muscles

49
Q

Somatostatin release is stimulated by

A

High fat, carbs, and protein rich meals

50
Q

Somatostatin receptors

A

SSTR2

found on both beta and alpha cells

51
Q

Somatostatin effects on pancreas

A

inhibits release of both insulin and glucagon by hyperpolarizing alpha/beta cells

52
Q

Somatostatin GI effects

A

“generalized inhibitory”

53
Q

Somatostatin on the hypothalamus

A

brain peptide, released into median eminence

Inhibits release of GH by anterior pituitary

54
Q

which hormone is decidedly not diabetogenic

A

Thyroid hormone

onset is too slow

55
Q

Hormones which are diabetogenic

A

Glucagon
Epinephrine
Cortisol
GH+IGF-1

56
Q

the brain

A

senses nutrients and hormones (insulin, leptin, GLP-1) associated with nutrient levels

57
Q

Epi and blood glucose

A

Increases glycogenolysis, gluconeogenesis

Increases glucagon, decreased insulin (a-adrenergic stimulation of beta cells)

58
Q

Cortisol and blood glucose

A

Increased gluconeogenesis

Increased glucose sparing (decreased uptake besides brain)

59
Q

Cortisol on the liver, early stage fasting:

A

promotes glycogenolysis

60
Q

Cortisol on the liver, late stage fasting:

A

promotes glycogen synthesis

61
Q

Growth hormone effect on blood glucose

A

glucose sparing

62
Q

Growth hormone effect on fatty acids

A

increased lipolysis

63
Q

Growth hormone effect on amino acids

A

Increased uptake into cells, decreased blood

64
Q

Growth hormone effect on muscle protein

A

Increased synthesis, increased DNA and RNA synthesis

decreased degradation

65
Q

Growth hormone released during

A

sleep
exercise
stress
hypoglycemia

66
Q

brain detects glucose in

A

Arcuate nucleus

67
Q

Hypothalamus and glucose homeostasis

A

Insulin and glucagon secretion

Hepatic glucose output

Glucose uptake by skeletal muscles