Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FHB Hormone/Repro > 80 - Pancreas > Flashcards

80 - Pancreas Flashcards

1
Q

Carbs, lipids, AA’s, and ketones can all be processed thru what catabolic pw?

A

TCA Cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What enzyme must be present for a cell to use ketone bodies for energy?

A

Thiophorase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Brain can only use ________ or ________ for energy source.

A

Glucose or ketone bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What’s a consequence of large accumulations of fat in organs, such as w/obesity?

A

Cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Is the majority of the pancreas endocrine or exocrine?

A

Exocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is the endocrine pancreas arranged?

A

Consists of 3 major cell types clustered in groups “islets of Langerhans”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 2 main cells of the endocrine pancreas, in order from largest to smallest amount? What about the other 3?
What does each cell secrete?

A
  1. Beta cells: 73-75%. Synthesize and secrete insulin.
  2. Alpha cells: 18-20%. Synthesize and secrete glucagon.
  3. Delta cells: 4-6%. Synthesize and secrete somatostatin (SS14).
  4. PP cells: (less than 1%): secrete pancreatic polypeptide.
  5. Epsilon cells (less than 1%): synthesize ghrelin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the function of PP? (endo/para/autocrine?)

A

Inhibit acinar cells via paracrine action.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What’s the other type of SS besides SS14 (released by delta cells of pancreas), and where is it released from?

A

SS28

- Released from stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the major, general functions of insulin and glucagon?

A
  • Insulin: energy storage (anabolic hormone)

- Glucagon: energy mobilization (catabolic hormone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Besides being produced by epsilon cells of the pancreas, ghrelin is produced in the stomach. What’s its fcn in the stomach?

A

Stimulates appetite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the blood flow pw of the islets of Langerhans?

What’s the hormonal significance of this?

A
  • Blood comes in thru arterioles, first contacts beta cells in “core”. Then, insulin rich blood reaches alpha cells in “mantle” (periphery) and leaves thru venules
  • Significance of “inside-out” flow: insulin affects glucagon, but not vice versa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the approx. half-life of insulin?

A

3-8 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Is insulin released alone or with another peptide?

A

W/ “C peptide”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the half-life of C peptide?

What is the significance of this?

A
  • 35 min

- Good, measurable indicator of pancreatic fcn (tells if insulin is being released from pancreas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why is C peptide synthesized w/proinsulin?

A

Essential for proper folding w/alpha and beta subunits of insulin (A and B), as well as di-S bond formation
- They are all packaged in storage vesicles together than then C peptide is removed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name the 5 steps of insulin release.

A
  1. Glucose xported into beta cell via GLUT-2
  2. Glucose P’lated by glucokinase; ATP generated
  3. ^[ATP] closes ATP-sensitive K+ channel
  4. Depolarization, Ca2+ channel opens
  5. Ca2+ influx causes exocytosis of insulin-containing vesicles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Does GLUT-2 have low or high glucose affinity?

A

Low, so this occurs when glucose conc is high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do sulfonylurea drugs specifically act on the process of insulin release?
What is the net effect?

A

The ATP-sensitive K+ channel has a SUR subunit

- Like ATP, sulfanylurea also close this channel, stimulating the release of insulin (DM tx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is known as the pancreatic “glucose sensor”?

A

Glucokinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How can FFAs/AAs influence the steps of insulin release from the beta cell?

A

They increase intracellular ATP, thus shutting off the K+ channel, depolarizing the cell, causing Ca2+ influx and exocytosis of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do incretins (GLP-1) influence insulin release from the beta cell?

A

They potentiate insulin release, but still need glucose!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do catecholamines influence insulin release from the beta cell?

A

Inhibition (act on alpha-adrenergic receptors of pancreas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Once a beta cell is stimulated via glucose infusion, describe the pattern of insulin secretion.

A

Biphasic

  1. Phase 1 is a spike (5% via docked and ready insulin-containing vesicles
  2. Phase 2 is a slower rise (95% via new synthesis and vesicle trafficking)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which of the 2 phases of insulin release is affected by DM?

A

1st phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What type of receptor is the insulin receptor?

- Name and describe its subunits

A

Receptor tyrosine kinase

  • Extracellular alpha subunit (w/hormone-binding domain)
  • Intracellular beta subunit w/ATP-binding and tyrosine kinase domain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

*Describe the process of insulin binding its receptor.
After, what is recruited and what do they do?
What’s the end result of all of this on a cell (e.g. skeletal myocyte)?

A
  • Insulin binds alpha subunit of receptor, causing autophosphorylation of intracellular beta subunit
  • Autophosphorylation of receptor recruits IRSs (insulin receptor substrates).
  • IRSs activate intracellular signaling cascades
  • End result: GLUT-4 inserted on membrane, glucose can enter cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the 2 key pathways that are stimulated upon insulin binding its receptor?

A
  1. PKB/PI3K pathway

2. MAPK pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

In insulin receptor stimulation, what is the PKB/PI3K pw a mediator of?
What other important protein is involved?

A

Main mediator of insulin’s metabolic effects.

- TC-10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

In insulin receptor stimulation, what is the MAPK pw a mediator of?

A

Main mediator of insulin’s growth and mitogenic effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Where is GLUT-1 found?

A

Brain vasculature, RBCs

  • Also SkM, fat, heart (minor)
  • Uptake under basal conditions
32
Q

Where is GLUT-2 found?

A

Pancreatic beta cells, liver, intestines, kidney

33
Q

Where is GLUT-3 found?

A

Neurons

34
Q

Which is the major transporter of glucose to the brain, GLUT-1 or GLUT-3?

A

GLUT-3

35
Q

Where is GLUT-4 found?

A

SkM, fat, stored inside cell under basal conditions

36
Q

Where is GLUT-5 found?

A

Spermatozoa, small intestine

37
Q

What does GLUT-5 uniquely do?

A

Xports fructose

38
Q

Which of the GLUTs are insulin-dependent?

A

GLUT-4 only!

39
Q

Which of the GLUTs are, importantly, saturated w/DM?

A

GLUT-2 (normally have low affinity for glucose)

40
Q

What are the physiological effects of insulin on the liver?

A
  • Increases glucose uptake
  • Promotes glycogen and TG production
  • Reduces glucose production/output (inhibits glucose-6 phosphatase and stimulates glucokinase synthesis- for liver)
41
Q

What are the physiological effects of insulin on the muscle?

A
  • Increases glucose uptake

- Promotes glycogen and TG production, protein synthesis

42
Q

What are the physiological effects of insulin on fat?

A
  • Increases glucose uptake
  • Promotes TG production, release of FFAs from chylomicrons, glycolysis
  • Inhibits lipolysis
43
Q

Besides glucagon, what else does preproglcagon have attached to it?

A
  • Signal sequence
  • GRPP
  • GLP-1, GLP-2
44
Q

Describe the products of preproglucagon released from the pancreas (not the stomach).

A
  • Inactive GRPP (co-peptide)
  • Active glucagon
  • Inactive GLP-1 bound to inactive GLP-2
45
Q

Describe the product of preproglucagon released from the intestinal L cells.

A
  • Inactive glicentin (glucagon + GRPP co-peptide)

- Active GLP-1 and GLP-2

46
Q

What does GLP stand for?

What is another name for GLP?

A
  • Glucagon-like peptide

- Incretin

47
Q

What are the effects of incretins?

A

Potentiate insulin release from pancreatic beta cells

48
Q

What, in the intestines, stimulates the release of GLP1/2?

A

Carbohydrates

49
Q

If you have a meal of pure carbohydrates, what will be secreted from the pancreas?

A

Insulin only

50
Q

What is the major counter-regulatory hormone to insulin?

A

Glucagon

- Most things that stimulate insulin will inhibit glucagon

51
Q

What 3 condition stimulates glucagon release from alpha cells?

A
  1. Low blood glucose
  2. Proteinacious meal
  3. Catecholamines (exercise)
52
Q

What are the 2 (not 3) main targets of glucagon?

A

Adipose and liver (not SkM- no receptors)

53
Q

(From big pic she uses lots of slides)

Overall, what are the effects of insulin?

A
  • ^ glucose uptake + utilization (m. + adipose)
  • v hepatic glucose production
  • ^ hepatic conversion of glucose to glycogen, lipids
  • Inhibit GNG
  • Inhibit HSTL, v release of FFA from adipose
54
Q

(From big pic she uses lots of slides)

Overall, what are the effects of glucagon?

A
  • ^ hepatic GNG and glycogenolysis
  • v hepatic conversion of glucose to glycogen/lipids
  • v uptake by adipose and muscle
  • ^ hepatic ketogenesis
  • ^ release of GNG substrates from m., adipose
  • ^ HSTL and release of FFA from adipose
55
Q

What do glucagon and insulin share, w/r/t how they act on enzymes?

A

Many act on the exact same enzymes

recall: glucagon/epi leads to P’lation, insulin is opposite

56
Q

What is specifically produced by delta cells in the pancreas?

A

Somatostatin 14 (SS14)

57
Q

What types of meal stimulate SS14 production?

What does SS14 do?

A
  • High fat, high carb

- Slows down digestive process

58
Q

How does insulin affect the production of SS14?

A

Inhibits it

59
Q

How does SS14 act on insulin release?

A

Suppresses it (not physiologically)

60
Q

What hormone is released w/insulin in beta cells?

A

Amylin

61
Q

What does amylin do?

A

Acts synergistically w/insulin

62
Q

Circulating amylin has been found to be increased in what 2 disease states?

A

Obesity, hypertension

63
Q

How might amylin be related to DM?

A

Possibly contributes to beta cell destruction by forming amyloid plaques

64
Q

How many AA’s is ghrelin?

A

28 AAs

65
Q

Most circulating ghrelin produced in the ________.

A

Stomach

66
Q

What does ghrelin do? (2 things)

A
  • Stimulates food intake at level of hypothalamus (hunger)

- Stimulates GH release (anticipates consumption of food)

67
Q

How are ghrelin levels related to obesity?

A

Inverse correlation between circulating ghrelin and obesity

68
Q

What newly described cells of the pancreas release ghrelin?

A

Epsilon cells

69
Q

How does pancreatic ghrelin act on pancreatic beta cells?

A
  • Inhibits insulin release via Gαi activation (opens) of K+ channels
  • Decreases intracellular Ca++; decreases insulin release
70
Q

Besides glucagon, what other hormones have a counter-regulator effect on insulin?

A
  • GH, cortisol

- Catecholamines

71
Q

How do cortisol and GH serve as counter-regulatory hormones to insulin?
How is IGF-I involved?

A
  • Permissive effects on GNG and lipolysis
  • Delayed response (6 hours): defense against prolonged hypoglycemia (starvation).
  • In absence of insulin, GH is elevated but cannot stimulate IGF-1. Result: direct glucose mobilization effects of GH, but no cellular proliferation effects of IGF-1. Also, no negative feedback to GH (cuz no IGF-I)
72
Q

How do catecholamines serve as counter-regulatory hormones to insulin?

A
  • Like glucagon, raise plasma glucose levels
  • Increased during exercise and stress
  • Inhibits insulin release directly at beta cell, stimulates glucagon in alpha cell
  • Increases hepatic glucose output
  • Decreases glucose uptake in skeletal muscle/adipose tissue
73
Q

If a normal, mixed meal of fats, carbs, and lipids, what is the balance b/w glucagon and insulin?
What about in an all protein meal?

A
  • More insulin than glucagon

- Glucagon only

74
Q

When insulin is present (read)…

A
  1. AA from protein stimulate GH which stimulates IGF-I (liver).
  2. IGF-I stimulates glucose uptake in muscle (like insulin), proliferation of visceral organ tissues; inhibits proteolysis.
  3. GH opposes insulin lipogenesis.
75
Q

What hormone would be clinically useful in managing insulin-producing tumors?

A

Somatostatin-14

FHB Hormone/Repro (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions