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GIGU Midterm > Endocrine Pancreas > Flashcards

Endocrine Pancreas Flashcards

1
Q

what is secreted in response to CHO- and/or protein ingestion?

A

insulin

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2
Q

what is the major stimulatory factor of insulin secretion?

A

glucose

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3
Q

what do the endocrine cells of the pancreas secrete?

A

insulin, glucagon, and somatostatin

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4
Q

how are the endocrine cells of the pancreas arranged?

A

in clusters known as islets of langerhans

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5
Q

what are the endocrine cells of the pancreas?

A

beta-cells, alpha-cells, delta-cells, and F-cells

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6
Q

what do the beta cells secrete?

A

insulin and C peptide

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7
Q

what do the alpha-cells secrete?

A

glucagon

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8
Q

what do the delta-cells secrete?

A

somatostatin

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9
Q

what do the F cells secrete?

A

pancreatic polypeptide

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10
Q

which cells are destroyed in a type 1 diabetic?

A

beta cells

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11
Q

what is the role of the F cells and their secretions?

A

they act like a satiety signal (neuropeptide Y, peptide YY family)

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12
Q

how do the endocrine cells of the pancreas/islets communicate with each other?

A

via gap junctions and blood supply

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13
Q

how does the arterial supply come into the islets?

A

it comes into the center and is going to primarily bathe the beta-cells

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14
Q

what kind of hormone is insulin?

A

peptide hormone

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15
Q

what is secreted at the same time as insulin?

A

C peptide

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16
Q

what does insulin signal the liver to do?

A

the liver senses the insulin and will stop producing glucose out into the bloodstream

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17
Q

how does glucose enter the beta-cell?

A

via GLUT-2

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18
Q

what happens once glucose enters the beta-cell?

A

it is phosphorylated by glucokinase into glucose-6-phosphate

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19
Q

what happens to the glucose-6-phosphate?

A

it is oxidized, which promotes ATP generation

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20
Q

what effect do the rising ATP levels have in the beta-cell?

A

ATP closes the “inward-rectifying” K+ channel (so the plasma membrane is a little more positive on the interior)

21
Q

what happens when the inward rectifying K+ channels are closed?

A

the plasma membrane is a little more positive on the interior–> the plasma membrane is depolarized

22
Q

what happens when the plasma membrane of the beta-cells is depolarized?

A

there is activation of the voltage-gated Ca2+ channels and Ca2+ enters the cell

23
Q

what happens when Ca2+ enters the beta-cells?

A

it initiates mobilization of insulin and C peptide containing vesicles to plasma membrane and exocytosis

24
Q

what drugs target the ATP-dependent K+ channels to increase insulin secretion?

A

sulfonylurea receptor drugs

25
Q

what is a general characteristic of insulin release?

A

it is biphasic- there is an initial spike within minutes and a further increase half an hour to an hour later

26
Q

what phase of insulin secretion is lost first in type 2 diabetics?

A

the first phase

27
Q

where does insulin resistance primarily occur?

A

adipose tissue and skeletal muscle

28
Q

what happens through AKT?

A

it signals to vesicles containing GLUT-4 to move to the plasma membrane and insert the GLUT-4 into the membrane. It then allows glucose to move into the cell, which will in turn lower the blood glucose levels

29
Q

what is a hypothesis on why the intracellular signaling gets “mucked up”?

A

mitochondrial overload- they have byproducts of metabolism that cause of family of stress kinases to inhibit and block what this intracellular signaling should do

30
Q

what happens to the incretin effect in T2DM?

A

it is abolished

31
Q

what are the stimulatory factors of insulin secretion?

A

increased glucose/amino acid/fatty acid/ketoacid concentration, glucagon, cortisol, GIP, CCK, GLP-1, vagal stimulation (ACh), sulfonylurea drugs

32
Q

what are the inhibitory factors of insulin secretion?

A

fasting, exercise, somatostatin, norepinephrine, diazoxide

33
Q

what effect does insulin have on K+?

A

there is an increased K+ uptake into the cells and therefore decreased K+ in the blood level

34
Q

what does muscle contraction activate?

A

AMP-Kinase (AMPK), which results in GLUT4 translocation to the plasma membrane and then glucose uptake

35
Q

what is the effect of glucagon?

A

it increases blood glucose levels

36
Q

what is the secretion of glucagon stimulated by?

A

decreased blood glucose (major), increased AAs, fasting, B-adrenergic agonists, ACh

37
Q

what inhibits glucagon?

A

insulin and high blood glucose levels and somatostatin

38
Q

what is the major factor contributing to development of T2DM?

A

multiple genes coupled with environment

39
Q

what ethnic group is more at risk for developing T2DM?

A

african americans, hispanic, and Pima native americans

40
Q

what happens when adipose tissue becomes inflammed?

A

they recruit macrophages, which then tell the adipocytes to become more dysfunctional and start releasing more inflammatory factors

41
Q

what are some pro-inflammatory cytokines?

A

IL-6, TNF-alpha, CRP

42
Q

what is the step after systemic insulin resistance?

A

reactive hyperinsulinemia- after eating a meal, glucose levels are normal but more insulin required

43
Q

what happens after hyperinsulinemia?

A

postprandial hyperglycemia

44
Q

when do symptoms become evident of T1DM?

A

not until ~80% of Beta cells are destroyed

45
Q

how do you get diabetic ketoacidosis (DKA)?

A

if there is decreased utilization of ketoacids

46
Q

besides inadequate insulin secretion, what else happens in T1DM patients?

A

hyperkalemia and osmotic diuresis

47
Q

is a family history more prominent for type 1 or type 2 diabetes?

A

type 2

48
Q

what is an example of a gene that is predominantly mutated in cases of T1DM?

A

DQ2/DQ8 gene

GIGU Midterm (19 decks)

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