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Block 3 Week 2 Meg > Insulin and Glucagon > Flashcards

Insulin and Glucagon Flashcards

1
Q

Autoimmune destruction of Beta cells

A

Type I diabetes

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2
Q

Beta cell exhaustion; compensation for insulin resistance

A

Type II diabetes

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3
Q

Which form of diabetes causes no insulin?

A

Type 1

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4
Q

Which form of diabetes causes not enough insulin?

A

Type 2

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5
Q

Diabetic complications

A 
Heart disease and stroke
High blood pressure
Blindness
Kidney disease
Nervous system disease
Amputation
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6
Q

The pancreas is composed of these two things

A

acini

islets of Langerhans

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7
Q

Islets of Langerhans secrete these two things into the blood

A

insulin

glucagon

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8
Q

What do alpha cells secrete?

A

glucagon

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9
Q

What do beta cells secrete?

A

insulin and amylin

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10
Q

What do gamma cells secrete?

A

somatostatin

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11
Q

Glucose homeostasis keeps blood glucose at what level?

A

5.5mM

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12
Q

Is insulin anti-hyperglycemic and anti-hypoglycemic?

A

Anti-hyperglycemic

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13
Q

What does somatostatin do for insulin and glucagon levels?

A

It is a tonic modulator, which means it keeps insulin and glucose levels within normal ranges

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14
Q

Proinsulin forms insulin and what other product?

A

C peptide

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15
Q

What can be used to measure insulin levels, because it doesn’t degrade as fast? It is secreted 1:1 with molecules of insulin.

A

C peptide

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16
Q

What test is administered to measure how glucose changes in blood over time?

A

oral glucose tolerance test

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17
Q

If blood glucose levels remain high, what occurs?

A

Glucose levels exceed the renal threshold for uptake, so you will pee out glucose

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18
Q

Does a meal always decrease glucagon secretion?

A

No

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19
Q

Compare the effect of a meal on glucagon vs insulin secretion.

A

After a meal, the change in glucagon levels are very minimal. However, changes in insulin levels are more drastic

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20
Q

Somatostatin acts as a (blank) and limits how much insulin and glucagon is secreted.

A

tonic inhibitor

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21
Q

During overnight fasting or between meals, what happens to lipolysis and lipogenesis?

A

lipolysis is stimulated; lipogenesis is inhibited

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22
Q

During overnight fasting or between meals, what happens to glucose storage in the liver (glycogen synthesis)?

A

It is inhibited

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23
Q

Does glucagon have an effect on peripheral tissues (muscle and adipocytes)?

A

No!

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24
Q

Fat cells do not have these receptors

A

glucagon receptors

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25
Q

Low insulin favors what and inhibits what?

A

Favors glycenolysis and inhibits glycogen synthesis.

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26
Q

During overnight fasting or between meals, resting glucose transport is decreased (blank)-fold relative to the fed state.

A

3-4 fold

27
Q

Low (blank) favors breakdown of glucose stores and inhibits formation of glucose stores in (blank).

A

insulin; muscle

28
Q

What can stimulate glucose transport to muscles when not in the “fed” state?

A

Exercise

29
Q

Very low levels of insulin are sufficient to inhibit breakdown of (blank)

A

fat

30
Q

Glucose transport into adipocytes is (blank)

A

VERY LOW

31
Q

What is the major site of glucose disposal after a meal?

A

Muscle

32
Q

During meals, what happens to glucose secretion? What happens to glucose storage?

A

Secretion is inhibited

Glucose storage is stimulated

33
Q

What happens to lipolysis during meals?

A

Inhibited

34
Q

High insulin increases glucose transport (blank) fold in muscle. Why is this essential?

A

four; for efficient glucose clearance from the blood

35
Q

What does high insulin do to glycogenolysis and glycogen synthase?

A

Stimulates glycogen synthase and inhibits glycogenolysis

36
Q

Very low levels of (blank) inhibit breakdown of fat.

A

insulin

37
Q

High insulin increases glucose transport (blank) fold in adipocytes.

A

20-50 fold

38
Q

How does glucose enter cells?

A

Through GLUT transporters

39
Q

Can G6P be transported through glucose transporters?

A

No

40
Q

In the liver, glucose phosphorylation is (blank) and the facilitative transporters are (blank)

A

reversible; non-directional

41
Q 
Discuss where the following transporters are found and their relative affinity:
Glut1
Glut 2
Glut 3
Glut 4
A

Glut 1: pancreatic alpha cells, high affinity (km=1mM)
Glut 2: pancreas and liver, low affinity (km=15mM)
Glut 3: brain, high affinity (km=0.4)
Glut 4: heart, skeletal muscle, and fat, high affinity and insulin dependent (km=1)

42
Q

At low blood glucose levels, there is (high/low) uptake of glucose into cells, (high/low) ATP/ADP ratio, (active/inactive) ATP/K+ channel, (active/inactive) Ca+ channel, release of insulin?

A

low; low; active; inactive; low

43
Q

At low glucose, is there a high or low ATP/ADP ratio?

A

low

44
Q

As glucose increases, what happens to the ATP/ADP ratio? What does this do to the ATP/K+ channel? What does this do to Ca+ channels? What does this do to insulin secretion?

A

it increases; inhibits ATP/K+ channel; activates Ca+ channels; increases insulin secretion

45
Q

Insulin secretion is low at basal glucose concentrations, because (blank) ratio is low

A

ATP/ADP

46
Q

Beta cells of the pancreas sense small changes in glucose, and these small changes are amplified. Why?

A

Glucose transporters on pancreas and liver have low affinity!

47
Q

In the beta cells of the pancreas, as glucose levels rise, what happens to the ATP/ADP ratio? Why?

A

It increases greatly, also the case in the liver; due to low affinity glucose transporters in pancreas and liver

48
Q

In the alpha cells of the pancreas, as glucose levels rise, what happens to the ATP/ADP ratio? Why?

A

It raises very slightly; due to high affinity glucose transporters

49
Q

The effect of changes in [glucose] on ATP/ADP are muted due to the high affinity of the glucose transporter isoform expressed in these cells

A

alpha cells

50
Q

Small changes in [glucose] are amplified due to the low affinity of the glucose transporter and glucose-kinase isoforms expressed in these cells

A

beta cells

51
Q

In the peripheral tissues (muscle and adipocytes), how is glucose transport rate limited?

A

By the total number of transporters inserted into the plasma membrane

52
Q

In the peripheral tissues, glucose transporters are nearly (blank) at basal [glucose].

A

saturated

53
Q

In what tissues is glucose transport rate limited by the total number of glucose transport proteins (GLUT4) in the plasma membrane?

A

In fat and muscle

54
Q

Oral hypoglycemic agents that inhibit KATP channels to increase insulin secretion

A

sulfonylureas

55
Q

What is the role of incretins in insulin secretion of beta cells?

A

they prime the vesicles with stored insulin to respond to increased Ca+

56
Q

This class of drugs inhibits the K-ATP channel in beta cells to increase the secretion of insulin. They are considered secretagogues.

A

sulfonylureas

57
Q

Which type of diabetes can be treated with hypoglycemics?

A

Type II

58
Q

Where is the highest affinity GLUT transporter found?

A

in the brain

59
Q

Four phases of glucose homeostasis during fasting

A
  1. fed: most of glucose is from food
  2. post-absorptive: most glucose is from glycogen breakdown and gluconeogenesis
  3. genic: most glucose is from gluconeogenesis by liver and kidneys
  4. prolonged: same as genic but lower levels of gluconeogenesis by liver and kidney
60
Q

During physical work, glucose uptake into the muscle (blank), and AMP kinase (blank) insulin secretion.

A

increases; decreases

61
Q

What is considered hyperglycemic? Normoglycemic? Hypoglycemic?

A

> 8mmol/l
5-8mmol/l
<3.8mmol/l

62
Q

Blood glucose exceeds renal threshold for uptake of glucose. Loss of glucose, water, Na+, K+ in urine.

A

Hyperglycemia

63
Q

Insulin secretion increases, which inhibits glucagon secretion

A

Normoglycemia

64
Q

Increases secretion of adrenaline and growth hormone in an attempt to raise blood sugar

A

Hypoglycemia

Block 3 Week 2 Meg (8 decks)

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