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FHB Exam 4: Endocrinology and Reproduction > Endocrine X: Pancreas > Flashcards

Endocrine X: Pancreas Flashcards

1
Q

What is a major metabolic byproduct of carbohydrate metabolism, and what is the implication?

A

ROS; over-production of ROS thought to be a root of diabetes complications, especially on the vasculature

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2
Q

What are the 2 main functions of the pancreas?

A

1) digestion (exocrine)

2) glucose regulation (endocrine)

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3
Q

What are some of the minor pancreatic hormones?

A

somatostatin (delta cells), amylin, pancreatic polypeptide (PP cells), ghrelin (epsilon cells)

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4
Q

What is the arrangement of alpha and beta cells in a pancreatic islet?

A

beta cells are clustered in the center; alpha cells are distributed outside (this arrangement allows for paracrine effects between the two)

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5
Q

What inhibits vs. stimulates alpha cells and glucagon release?

A

insulin inhibits, catecholamines stimulate

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6
Q

Why is cleavage of C peptide from insulin critical?

A

It exposes the end of the insulin chain that interacts with the receptor.

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7
Q

If insulin is injected into someone, will C-peptide be present?

A

No, because when insulin is injected it is in the active form. C-peptide is only associated with endogenously produced insulin.

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8
Q

Which glucose transporter is insulin-dependent?

A

GLUT4

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9
Q

Which glucose transporter is expressed on the surface of pancreatic beta cells?

A

GLUT2

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10
Q

Does GLUT2 have a low or high affinity for insulin?

A

low affinity; only when glucose is high will it transport

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11
Q

Which enzyme is known as the “pancreatic glucose sensor”?

A

glucokinase

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12
Q

What happens on an ion/transporter level for insulin to be released?

A

increased ATP production via intracellular metabolism of glucose binds to K+ channels and closes them; increased K+ inside of the cell causes depolarization of the cell, which opens voltage-gated Ca2+ channels; Ca2+ influx causes exocytosis of insulin-containing vesicles

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13
Q

Why is insulin released in a biphasic manner?

A

because only 5% of vesicles are docked at the membrane and available for immediate release; the remaining 95% are “stored” and must be mobilized via intracellular signaling

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14
Q

Describe the insulin receptor.

A
  • receptor tyrosine kinase with 2 alpha and 2 beta subunits held together by disulfide bonds
  • insulin binds at alpha subunit on extracellular side
  • beta subunit on cytoplasmic side is autophosphorylated upon insulin binding
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15
Q

What happens once insulin receptors are autophosphorylated?

A

recruitment of IRSs (insulin receptor substrates), which activate intracellular signaling cascades by creating a scaffold

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16
Q

What are some of the anabolic actions of insulin?

A
  • utilization of glucose for ATP
  • storage of FFAs as TGs
  • protein synthesis from aa’s
  • macromolecular synthesis
  • organelle formation
  • cell proliferation
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17
Q

Which pathways does IRS protein stimulate?

A
  • Akt pathway (stimulating metabolic actions)

- MAPK/ERK pathway (stimulating mitogenic and metabolic actions)

18
Q

Where does GLUT4 translocation occur, and what is it stimulated by?

A

occurs in muscle and adipose tissue; stimulated by Akt signaling pathway

19
Q

Which is the major glucose transporter in the brain?

A

GLUT3

20
Q

Which glucose transporter causes uptake of glucose under basal conditions?

A

GLUT1

21
Q

Which glucose transporter does insulin resistance affect and why?

A

GLUT4 transporter, as it is insulin-dependent

22
Q

What is the major physiological effect of insulin on adipose tissue?

A

promotes TG production and release of FFAs from chylomicrons; inhibits lipolysis

23
Q

What is the major physiological effect of insulin on muscle?

A

promotes glycogen and TG production, as well as protein synthesis

24
Q

What is the major physiological effect of insulin on the liver?

A

promotes glycogen and TG production and reduces glucose production/output

25
Q

What is the overall primary action of insulin on its target cells?

A

energy storage!

26
Q

Which enzymes does glucose affect in the liver?

A
  • inhibits glucose-6-phosphatase (therefore, gluconeogenesis is inhibited)
  • stimulates glucokinase (traps glucose within the cell for storage)
27
Q

What is responsible for shuttling glucose into and out of hepatocytes?

A

GLUT2 transporter

28
Q

How is glucagon synthesized?

A

It is a peptide hormone that is first synthesized as preproglucagon

29
Q

What are some of the byproducts of biosynthetic processing of glucagon?

A

incretins, like GLP-1 and GLP-2, as well as GRPP (secreted as an inactive peptide)

30
Q

What is proglucagon made up of?

A

glucagon, GRPP, GLP-1, and GLP-2

31
Q

What is the function of incretins?

A

potentiate insulin release

32
Q

What stimulates glucagon release?

A

amino acids (protein meals)

33
Q

Incretins are a drug target for _____.

A

T2DM (“Januvia”)

34
Q

What are incretins degraded by?

A

DPP-4 enzyme

35
Q

The majority of insulin release is due to which nutrient?

A

carbohydrates

36
Q

Which hormone(s) directly inhibit insulin release from beta cells?

A

epi/norepi through activation of alpha2-adrenergic receptors

37
Q

What are the main targets of glucagon?

A

liver and adipose tissue; no glucagon receptors in skeletal tissue

38
Q

What are the main counter-regulatory hormones to insulin?

A

1) Glucagon (primary)
2) GH and cortisol (permissive effects on gluconeogenesis and lipolysis) - delayed response and defense against prolonged hypoglycemia

39
Q

Do obese patients have higher or lower levels of circulating ghrelin?

A

lower levels because stomach is perpetually stretched; theoretically, obese patients should not be as hungry as patients with a normal weight, but this is not observed due to other modulatory effects of CNS

40
Q

What is the effect of somatostatin on insulin?

A

inhibits insulin; can be used for management of insulin-producing tumors

41
Q

What is the function of amylin?

A

It is released with insulin from vesicles in beta cells and is synergistic with insulin in the regulation of blood glucose.

42
Q

How is amylin related to diabetes?

A

It may be a contributing factor to beta cell destruction by forming amyloids. Circulating amylin is also increased in those with obesity.

FHB Exam 4: Endocrinology and Reproduction (14 decks)

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