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
Low insulin favors what and inhibits what?
Favors glycenolysis and inhibits glycogen synthesis.
26
During overnight fasting or between meals, resting glucose transport is decreased (blank)-fold relative to the fed state.
3-4 fold
27
Low (blank) favors breakdown of glucose stores and inhibits formation of glucose stores in (blank).
insulin; muscle
28
What can stimulate glucose transport to muscles when not in the "fed" state?
Exercise
29
Very low levels of insulin are sufficient to inhibit breakdown of (blank)
fat
30
Glucose transport into adipocytes is (blank)
VERY LOW
31
What is the major site of glucose disposal after a meal?
Muscle
32
During meals, what happens to glucose secretion? What happens to glucose storage?
Secretion is inhibited | Glucose storage is stimulated
33
What happens to lipolysis during meals?
Inhibited
34
High insulin increases glucose transport (blank) fold in muscle. Why is this essential?
four; for efficient glucose clearance from the blood
35
What does high insulin do to glycogenolysis and glycogen synthase?
Stimulates glycogen synthase and inhibits glycogenolysis
36
Very low levels of (blank) inhibit breakdown of fat.
insulin
37
High insulin increases glucose transport (blank) fold in adipocytes.
20-50 fold
38
How does glucose enter cells?
Through GLUT transporters
39
Can G6P be transported through glucose transporters?
No
40
In the liver, glucose phosphorylation is (blank) and the facilitative transporters are (blank)
reversible; non-directional
41
``` Discuss where the following transporters are found and their relative affinity: Glut1 Glut 2 Glut 3 Glut 4 ```
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
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?
low; low; active; inactive; low
43
At low glucose, is there a high or low ATP/ADP ratio?
low
44
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?
it increases; inhibits ATP/K+ channel; activates Ca+ channels; increases insulin secretion
45
Insulin secretion is low at basal glucose concentrations, because (blank) ratio is low
ATP/ADP
46
Beta cells of the pancreas sense small changes in glucose, and these small changes are amplified. Why?
Glucose transporters on pancreas and liver have low affinity!
47
In the beta cells of the pancreas, as glucose levels rise, what happens to the ATP/ADP ratio? Why?
It increases greatly, also the case in the liver; due to low affinity glucose transporters in pancreas and liver
48
In the alpha cells of the pancreas, as glucose levels rise, what happens to the ATP/ADP ratio? Why?
It raises very slightly; due to high affinity glucose transporters
49
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
alpha cells
50
Small changes in [glucose] are amplified due to the low affinity of the glucose transporter and glucose-kinase isoforms expressed in these cells
beta cells
51
In the peripheral tissues (muscle and adipocytes), how is glucose transport rate limited?
By the total number of transporters inserted into the plasma membrane
52
In the peripheral tissues, glucose transporters are nearly (blank) at basal [glucose].
saturated
53
In what tissues is glucose transport rate limited by the total number of glucose transport proteins (GLUT4) in the plasma membrane?
In fat and muscle
54
Oral hypoglycemic agents that inhibit KATP channels to increase insulin secretion
sulfonylureas
55
What is the role of incretins in insulin secretion of beta cells?
they prime the vesicles with stored insulin to respond to increased Ca+
56
This class of drugs inhibits the K-ATP channel in beta cells to increase the secretion of insulin. They are considered secretagogues.
sulfonylureas
57
Which type of diabetes can be treated with hypoglycemics?
Type II
58
Where is the highest affinity GLUT transporter found?
in the brain
59
Four phases of glucose homeostasis during fasting
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
During physical work, glucose uptake into the muscle (blank), and AMP kinase (blank) insulin secretion.
increases; decreases
61
What is considered hyperglycemic? Normoglycemic? Hypoglycemic?
>8mmol/l 5-8mmol/l <3.8mmol/l
62
Blood glucose exceeds renal threshold for uptake of glucose. Loss of glucose, water, Na+, K+ in urine.
Hyperglycemia
63
Insulin secretion increases, which inhibits glucagon secretion
Normoglycemia
64
Increases secretion of adrenaline and growth hormone in an attempt to raise blood sugar
Hypoglycemia