Brainscape's Knowledge GenomeTM

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


See full index

Endo/Repro: Week 2 > Rose: Endocrine Pancreas > Flashcards

Rose: Endocrine Pancreas Flashcards

1
Q

Where is glucose stored for future energy needs after feeding?

A

Liver and muscle= stored as glycogen (lasts 12 hrs)

adipose tissue= stored as TG (unlimited)

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

Does the brain store energy?

A

No

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

How does the body store glucose in the fed state?

A

as glycogen and TG

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

What processes occur after eating?

A 
LIPOGENESIS: 
glucose> 
2 pyruvates> 
citrate>
FFA+ glycerol>
TG

GLYCOGENESIS:
glucose>
glycogen

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

What is the role of insulin in the FED state?

A
  1. inhibits intracellular lipases (hydrolyze TG)> inhibits brkdwn of fat/adipose
  2. Facilitates entry of glucose into adipocytes and liver> promotes accumulation of TG in fat cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is glucose used for in adipose?

A

used to synthesize glycerol

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

What is glucose used for in the liver?

A

FA (only once glycogen stores are maximal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens to liver derived FA?

A 
packaged as lipoproteins>
enter circulation as FA>
picked up by Adipose>
combined w/ glycerol>
TG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What procceses increase in the FED state when INSULIN predominates?

A

↑ glucose oxidation (= glycolysis)
↑ glycogen synthesis
↑ fat synthesis
↑ protein synthesis

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

What processes increase in the FASTED state when GLUCAGON predominates?

A

↑ glycogenolysis
↑ gluconeogenesis
↑ ketogenesis

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

What pancreatic islet hormones regulate glucose levels?

A

β cell (70%): Insulin and amylin

α cell (20%): Glucagon is dominant with fasting

δ cell (5%): Somatostatin

ε cell (<1%): Ghrelin

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

What inhibits insulin secretion during fight/flight?

A

SNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What type of innervation is involved in the cephalic phase of insulin secretion?

A

PNS

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

What hormone dominates in the Fasted state? What biochemical process dominates in the fastest state?

A

glucagon

gluconeogenesis

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

What is gluconeogenesis?

A

glucose production from noncarbohydrate sources, glycerol, and amino acids

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

What is the preferred energy source for the brain?

A

Glucose

ketones in starvation

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

What gets broken down in the fasted state to maintain glucose levels??

A

1st- Glycogen breakdown in liver & muscle → glucose (reserves depleted in 24 hrs)

2nd – Adipose TGs are catabolized to glycerol and FFAs

3rd – glycerol made into glucose (gluconeogenesis in the liver) and FFAs, acetoacetate and b-hydroxybuterate can be made in the liver.

4th- muscle wasting (proteins catabolized> AA> gluconeogenesis in the liver> Glucose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How are ketones metabolized?

A

Ketones converted to acetyl CoA → energy in the citric acid cycle in tissues including brain and muscle

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

What can be measured as an indicator of endogenous insulin production in diabetic pts?

A

C peptide (connecting peptide)

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

What is the t1/2 of insulin and where is it metabolized?

A

circulates FREE in the plasma for

metabolized by the kidney and liver

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

What type of receptor is the insulin receptor?

A

tyrosine kinase

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

What does amylin do?

A

Copackaged/secreted w/ insulin from beta cell>

inhibits glucagon secretion at the level of the alpha cell

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

How does amylin affect satiety?

A

induces satiety by:

↓ food intake, delay gastric emptying, and inhibiting secretion of digestive enzymes, stomach acid, and bile ejection

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

What hormone promotes liver gluconeogenesis, glycogenolysis and lipolysis?

A

Glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where is glucagon produced?

A

alpha cell of pancreas

synthesized as proglucagon> spliced into glucagon

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

What leads to increased glucagon?

A

hypoglycemia
AA (protect from hypoglycemia after a protein meal)
SNS and vagal stimulation (tempers insulin affects)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What leads to decreased glucagon?

A

hyperglycemia

amylin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What type of receptor is the glucagon receptor?

A

GPCR

29
Q

What does somatostatin do?

A

inhibits production of pancreatic hormones (insulin, glucagon, ghrelin)

30
Q

What stimulates somatostatin?

A

increase in insulin

31
Q

What inhibits STT?

A

ghrelin

32
Q

How does STT affect the GI tract?

A

decreases the rate of food absorption

33
Q

When is Ghrelin active and what does it do?

A

Increases w/ fasting>

promotes glucagon secretion and inhibits insulin and STT

34
Q

What are incretins?

A

GI hormones that promote insulin release after eating

35
Q

What do incretins (GI HORMONES) do?

A

DECREASE gastric emptying> SLOWs rate of absorption of nutrients into blood stream

*may also directly decrease food intakes

36
Q

What stimulates insulin in a high glucose situation?

A

GLP-1

37
Q

Where is GLP-1 produced?

A

PROGLUCAGON GENE> cleaved in intestinal cells>
GLP-1>
secreted from L cells of lower SI and colon

38
Q

What is GLP-1 degraded by?

A

dipeptidyl peptidase-4

39
Q

What produces GIP?

A

K cells of duodenum and jejunum

40
Q

What is the t1/2 like for GIP and GLP-1?

A

mins

41
Q

What are the 4 phases of insulin secretion?

A

1) Cephalic Phase- PNS info from sight and smell
2) Oral Phase- PNS info and carb sugar stimulation of sweet receptors
3) GI Phase
o The “incretins”
4) Blood Glucose Phase
o ↑ in blood glucose triggers β cell release of insulin
o ↓ in blood glucose triggers α cell release of glucagon

42
Q

How

A

1) Cephalic Phase- parasympathetic info from sight and smell
2) Oral Phase- parasympathetic info and carb sugar stimulation of sweet receptors
3) GI Phase
o The “incretins”
— GIP: produced in response to hyperosmolarity d/t glucose in gut; Amt of insulin secreted is greater when glucose is administered orally than IV
— GLP-1 (remember: derived from a proglucagon gene)
4) Blood Glucose Phase
o ↑ in blood glucose triggers β cell release of insulin
o ↓ in blood glucose triggers α cell release of glucagon

43
Q

What happens to the incretins during the GI phase?

A

GIP: produced in response to hyperosmolarity d/t glucose in gut; Amt of insulin secreted is greater when glucose is administered orally than IV

GLP-1 (remember: derived from a proglucagon gene)

44
Q

What is the incretin effect? What causes it?

A

When you get a larger response from oral vs. IV glucose.

D/t the oral and intestinal phases of insulin secretion (parasympathetic and incretin signals)

45
Q

What controls nutrient intake and nutrient influx to the blood by inhibiting food intake and gastric emptying (also inhibits glucagon secretion)?

A

Beta cell secretion of amylin and insulin

46
Q

What is made in the distal small bowel and colon in response to glucose and acts on receptors in beta pancreatic cells and the brain?

A

GLP-1

47
Q

What is made by intestinal K cells in response to glucose and acts on receptors in beta pancreatic cells and in the brain.

A

GIP

48
Q

What increases insulin secretion when there are high levels of glucose?

A

GIP

49
Q

What do epsiolon cells do?

A

secrete ghrelin>

promotes glucagon stimulation (hunger signal that coincides w/ low glucose)

50
Q

What inhibits secretion of insulin, glucagon, and ghrelin and is stimulated by insulin release (part of neg. feedback to ensure hormones do not overshoot)?

A

STT

51
Q

How do you prevent hypoglycemia?

A

glucagon

52
Q

What are the two types of glucose transporters involved in maintaining glucose homeostasis?

A

SGLTs and GLUTs

53
Q

How do SGLTs work and where are they located?

A

Active transporters/symporters in the gut/kidney that derive energy for transport from the Na gradient across the membrane.

54
Q

What is one way to block glucose reabsorption?

A

block SGLT1 or SGLT2

55
Q

How does SGLT2 allow for the passive diffusion of glucose out of the cell and DOWN the gradient?

A

Na+ equilibrium maintained by Na+/K+ ATPase on basolateral surface

Na+ DOWN gradient allows for glucose to be transported UP it’s gradient into the cell

56
Q

Where is SGLT located?

A

KIDNEY

57
Q

What type of transporters are GLUTs?

A

facilitated transporters

58
Q

What are the 3 classes of Gluts?

A

I, II, and III

59
Q

What GLUT transporter is responsible for the LOW level basal uptake of glucose that occurs in MOST cells?

A

GLUT 1

60
Q

What GLUT transporter acts as a “glucose sensor” in the pancreas and initiates the secretion of insulin?

A

GLUT 2

61
Q

Where is GLUT 2 located?

A

Liver, beta cells, kidney, hypothalamus, basolateral membrane small intestine.

62
Q

What GLUT is located in skeletal and cardiac muscle and fat is and is activated by INSULIN?

A

GLUT4

63
Q

What is PULSATILE insulin secretion dependent on?

A

Calcium!!

64
Q

How is insulin secretion Ca dependent? Describe the mechanism.

A

Cholinergic stimulation (ACh) d/t metabolism of nutrients
→ CLOSES an ATP-sensitive K+ channel
→ depolarizes pancreatic b-cell
→ extracellular Ca2+ enters via voltage-dependent Ca2+ channel
→ stimulates secretion of insulin

65
Q

Besides CHOLINERGIC stimulation, what are other STIMULATORS of insulin secretion?

A

Cholinergic stimulation
Glucagon (provides “fine tuning” the steady-state levels of blood glucose → prevents wide fluctuations)
Amylin, GLP-1, GIP, gastrin, secretin, and CCK

66
Q

Besides ADRENERGIC stimulation, what are other INHIBITORS of insulin secretion?

A

Catecholamines

SST

67
Q

Describe insulin signaling.

A

1) Insulin binds tyrosine kinase receptor ↑ glucose storage as glycogen or TGs
2) Receptor phosphorylates insulin-receptor substrates (IRS)
3) 2nd messenger pathways alter protein synthesis and existing proteins
4) Membrane transport is modified
5) Cell metabolism is changed

68
Q

What induces the exocytosis of GLUT4 transporters?

A

INSULIN

exercise

Endo/Repro: Week 2 (11 decks)

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