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Block 3 Week 2 Dani > Mastick BCH Insulin and Glucagon > Flashcards

Mastick BCH Insulin and Glucagon Flashcards

1
Q

What is this:

autoimmune destruction of beta cells

A

Type 1 diabetes

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2
Q

What is this:

B cell exhaustion; compensation for insulin resistance

A

Type II diabetes

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3
Q

What is the primary defect of type 1 diabetes and how do fix this?

A

No insulin

insulin injections required or islet transplant

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4
Q

What is the secondary defect of type 2 diabetes?

How do you fix this?

A 
not enough insulin 
oral hypoglycemics (work to lower your blood sugar)
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5
Q

Where in the US is diabetes the worst?

A

the south

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6
Q

The diabetes epidemic has turned into the diabetes tsunami because a ….

A

higher percentage of pop are becoming diabetic

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7
Q

(blank) % of the population have diabetes

A

8.3%

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8
Q

What are complication associated with diabetes?

A 
heart disease and stroke
high blood pressure
blindness
kidney disease
nervous system disease (neuropathy)
amputation
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9
Q

What endocrine hormones does the pancreas secrete?

A

insulin, glucagon, somatostatin

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10
Q

(blank) is richly vascularized and innervated by sympathetic and parasympathetic fibers.

A

pancreas

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11
Q

What are the 2 components of the pancreas?

A

acini and islets of langerhans

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12
Q

What secrete digestive juices into duodenum?

A

acini

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13
Q

What secrete insulin and glucagon into blood (separated from the acini by CT capsule)?

A

Islet of Langerhans

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14
Q

What are the three types of cells that the islets of langerhan contain?
What is the most abundant?

A

Alpha cells
beta cells
delta cells
Beta cells are the most abundant

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15
Q

TO maintain glucose homeostasis, blood glucose levels should be at around (blank)

A

5.5

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16
Q

(blank) is an anti-hyperglycemic

A

insulin

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17
Q

(blank) is an anti-hypoglycemic

A

glucago

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18
Q

(blank) is a tonic modulator

A

somatostatin

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19
Q

What keeps levels of the secretion of insulin and and glucagon constant?

A

somatostatin

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20
Q

Explain what happens to proglucagon

A

Proglucagon can either leave the ER and go into vesicles to become glucagon in pancreatic islet alpha cells or can go into intestinal L cells and STN neurons to become oxyntomodulin

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21
Q

Explain what happens to preproinsulin?

A

Pre form allows (preproinsulin) of insulin allows the pro form to be folded properly, it is cleaved and becomes insulin and a C peptide

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22
Q

(blank) has a short half life.

A

Insulin

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23
Q

(blank) levels are measured to see insulin levels due to the fact that they are in the same secretory granules and are in a one to one ratio with insulin.

A

C peptide

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24
Q

What three cell types are intercalated and communicate with each other?

A

insulin, glucagon, somatostatin

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25
Q

What are the four phases of glucose homeostasis during fasting?

A

well fed
post absorptive
gluconeogenic (early)
prolonged

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26
Q

When you have prolonged fasting up to 42 days what happens to your glucose levels?

A

they remain relatively stable and steady

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27
Q

When you eat what happens to your glycogen levels? WHen you start to use up your glycogen what happens?

A

They increase

you start to increase gluconeogenesis

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28
Q 
During phase 1:
What is the nutritional status?
What is the origin of the blood glucose?
What tissues are using glucose?
What is the major fuel of the brain?
A

well fed
exogenous
all
glucose

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29
Q 
During phase 2:
What is the nutritional status?
What is the origin of the blood glucose?
What tissues are using glucose?
What is the major fuel of the brain?
A
  • post-absorptive
  • hepatic glycogen, gluconeogenesis
  • all except liver. Muscle and adipose at diminished rates
  • glucose
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30
Q 
During phase 3:
What is the nutritional status?
What is the origin of the blood glucose?
What tissues are using glucose?
What is the major fuel of the brain?
A

gluconeogenic (early)
hepatic and renal gluconeogenesis
Brainand RBCs; small amount by muscle
glucose, ketone bodies

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31
Q 
During phase 4:
What is the nutritional status?
What is the origin of the blood glucose?
What tissues are using glucose?
What is the major fuel of the brain?
A

Prolonged
renal and hepatic gluconeogenesis
RBCs, Brain at dimished rate
ketone bodies, glucose

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32
Q

What happens if glucohomeostasis fails?

A

death

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33
Q

If your blood glucose level is above 8 whats up?

A

hyperglycemia !!!

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34
Q

If your blood glucose levels are slightly higher than 5.5 whats up?

A

normoglycemia fed state; insulin secretion increase which inhibits glucagon secretion

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35
Q

If your blood glucose levels are at 5.5 whats up?

A

normoglycemia fasting

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36
Q

If your blood glucose levels are at 4.6 whats up?

A

normoglycemia under a load (heavy physical exercise) insulin secretion decreases, which causes glucagon secretion to increase

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37
Q

If you are at 3.8 glucose whats up?

A

hypoglycemia, increase secretion of adrenaline and growth hormone

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38
Q

What are these:

  1. 2 Cortisol secretion.
    2. 8 Confusion.
    1. 7 Weak, sweat, nauseous.
    1. 1 Muscle cramps.
    0. 6 Brain damage, death.
A

problems arising from decreased blood glucose

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39
Q

What does a glucose tolerance test do and how does it work?

A

adults are given 75g of glucose and some water.
Watch reaction
Normal: glucose levels remain below 200
Diabetes: glucose levels are higher than 200

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40
Q

What is this:

Exceeds renal threshold for uptake of glucose from pre-urine, diuresis (loss of glucose, water, Na+and K+ in urine).

A

hyperglycemia

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41
Q

Is acute hyperglycemia life threatening?

A

no the problem arises to chronic exposure to glucose

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42
Q

(blank) is reactive and inactives proteins and such so it can cause a lot of complications.

A

glucose

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43
Q

Does a meal always decrease glucagon secretion?

A

no

44
Q

When a meal decreases glucagon secretion, is the effect big or small?

A

small!

45
Q

Under normal circumstances, when you have a meal your (blank) levels will change a lot and your (Blank) levels will only change slightly

A

insulin

glucagon

46
Q

A high (blank) meal increases the secretion of both glucagon and insulin

A

protein (or arginine)

47
Q

(blank) percent of glucose goes to brain

A

60%

48
Q

Alpha cells make (blank) and beta cells make (blank)

A

glucagon

insulin

49
Q

During an overnight fast, the insulin/glucagon ratio favors (blank)

A

glucose secretion (glycogenolysis, gluconeogenesis)

50
Q

During an overnight fast, glucose storage is (blank) in the liver

A

inhibited

51
Q

During an overnight fast, lipolysis is (blank) and lipogenesis is (blank)

A

stimulated

inhibited

52
Q

Is there an effect on glucagon on peripheral tissues?

A

NOOOO only liver

53
Q

During an overnight fast, low (blank) favors breakdown of glucose stores(glycogenolysis) and inhibits formation of glucose stores in (Blank). This reduces the amount of glucose required from the blood.

A

insulin

54
Q

Resting glucose transport is decreased 3-4 fold relative to the fed (high insulin) state, but can be fully stimulated by (blank)

A

exercise or other stimuli AMPK

55
Q

If muscles are being pushed (higher energy states) then high (blank) will stimulate glucose transport from blood

A

AMPK

56
Q

Glucose incorporation into triglyceride (lipogenesis) is (blank) by glucose transport in adips. No hormones are required to maintain low basal rate.
(adipocytes are full of energy, dont really care about getting glucose)

A

rate limited

57
Q

(blank) is the major site of glucose disposal after a meal

A

muscle

58
Q

During fed metabolic state (prandial/during meals), insulin/glucagon ratio inhibits (blank) secretion and stimulates (blank) in the liver.

A

glucose

glucose storage

59
Q

During the fed state (blank) is inhibited.

A

lipolysis

60
Q

(blank) increases glucose transport 4-fold in muscle. This is rate limiting, and stimulation of this step is essential for efficient glucose clearance from the blood.

A

high insulin

61
Q

Glucose transport to the muscles can be fully stimulated by (blank) even in insulin resistant states

A

exercise

62
Q

High insulin stimulates (blank) and inhibits (blank) in the muscle.

A 
glucose storage (glycogen synthesis)
 glycogen breakdown (glyogenolysis)
63
Q

(blank) increases glucose transport 20-50-fold in adipocytes!

A

High insulin

64
Q 
Very low (basal fasting) levels of insulin are sufficient to (blank) breakdown of fat (lipolysis) in adipose tissue.
 Therefore what is needed to stimulate lipolysis in fat?
A

inhibit

other hormones

65
Q

extreme exercise can cause (blank)

A

hypoglycemia

66
Q

PP1 does what?

A

Turns glucose into glycogen or fat

67
Q

What does PKA do?

A

Turns glycogen into glucose

68
Q

GLucose enters cells through (blank)

A

facilitative GLUTs

69
Q

TO keep glucose inside of cell once it is transported, there are enzymes inside the cell that (blank) the glucose (hexokinase or glucokinase) which will make it so that glucose is stuck inside cell. So you have very low levels of free glucose in cell because it is phosphorylated so quickly. Is this reversible?

A

phosphorylate

ONLY in liver!!! No where else

70
Q

What transporter has highest affinity?

A

glut 3 for the brain

71
Q

What transporter has low affinity?

Do they work at max efficiency?

A 
Glut 2 (liver, pancreatic b cells, intestine)
NO
72
Q

What receptors do you find on skeletal and fat?

A

high affinty GLUT 4

73
Q

Where do you find glut 1 and is it high or low affinity

A

high

pancreatic alpha cells and most other tissues

74
Q

(blank) secretion is low at basal glucose concentrations, high at fed glucose levels

A

Insulin

75
Q

(blank) secretion is low at basal glucose concentrations, because ATP/ADP ratio is low.

A

insulin

76
Q

At low glucose, there is a low (blank) ratio

A

ATP/ADP

77
Q

What happens when you have low glucose?

A

Low glucose->Low ATP-> K channel active-> Ca channel inhibited-> insulin secretion is inhibited

78
Q

What happens when you have high amounts of glucose?

A

High ATP-> inhibition of K channel-> activation of Ca channel-> increase in insulin secretion

79
Q

(blank) secretion increases as the [glucose] increases and the ATP/ADP ratio increases

A

Insulin

80
Q

What is this:
small changes in [glucose] are amplified due to the low affinity of the glucose transporter and glucose-kinase isoforms expressed in β cells

A

glucose sensing

81
Q

(blank) is a Low affinity (Km = 15 mM), high capacity glucose transporter

A

GLUT 2

82
Q

(blank) is a low affinity (Km = 10 mM), high capacity kinase

A

Glucokinase

83
Q

(blank) is also dependent on the ATP/ADP ratio in α cells, but this does not change
much at physiological glucose concentrations!

A

glucose sensing

84
Q

(blank) is a High affinity (Km = 1 mM), low capacity glucose transporter
Glucokinase- low affinity (Km = 10 mM), high capacity kinase

A

GLUT1

85
Q

Glucose sensing: the effect of changes in [glucose] on ATP/ADP are muted due to the
high affinity of the glucose transporter isoform expressed in (blank)

A

α cells

86
Q

There are (blank) mechanisms of control of glucagon secretion

A

multiple alternative mechanisms

87
Q

In peripheral tissues, glucose transport is rate limited by the total number of (blank)
inserted into the plasma membrane (each is working at maximum capacity)

A

transporters

88
Q

(blank) - High affinity (Km = 1 mM), low capacity glucose transporter
(blank) - High affinity (Km = 10 μM), low capacity kinase

A

GLUT4

Hexokinase

89
Q

Insulin stimulates glucose transport in (blank) 20-50 fold, but only 3-4 fold in
(blank).

A

fat

muscle

90
Q

The (blank) are nearly saturated at 4 mM glucose, therefore, there is no change in glucose uptake in cells expressing these transporters under normal physiological blood glucose levels UNLESS the total number of glucose transport proteins at the cell surface changes (GLUT4, the insulin-responsive transporter).

A

The high affinity glucose transporters (GLUTs 1,3,4

91
Q

The (blank) is not saturated at physiological blood glucose concentrations, therefore, glucose uptake changes over all ranges of physiological glucose in cells expressing these transporters (beta cells and liver).

A

the low affinity glucose transporter GLUT 2

92
Q

Why do you need a tonic regulator if it is the insulin/glucagon ratio that determines
the flux of glucose into and out of the blood?

A

YOu would get out of control high levels of these hormones without a tonic regulator

93
Q

(blank)

Acts as tonic inhibitor- limits how much of both are released, but does not affect when

A

somatostatin

94
Q

(blank) Work directly on the ATP sensitive potassium channel. They inhibit this channel which allows calcium to flow in which allows direct stimulation of insulin secretion into the blood from pancreatic beta cells

A

sulfonylureas

95
Q

(blank) work at level o beta cell-> bind to specific receptor on beta cells and make the cell more susceptible to stimulation to secrete insulin

A

incretins

96
Q

What do these do:
 Sulfonylureas (Diabeta, Glucotrol, Amaryl)- KATP channel modulators β- CELLS

 Other Secretagogues (Starlix, Prandin)- KATP channel modulators β- CELLS

 Incretin analogues (Exendin-4, Exenatide)- GLP-1 receptor agonists β- CELLS

 DPP-4 Inhibitors (Januvia, Onglyza)- slows incretin turnover β- CELLS

A

increased insulin secretion

97
Q

What do these do:
Biguanides (Metformin)- activates AMPK (indirect), insulin sensitizer MUSCLE

 Thiazolidinediones (Avandia, Actos)- PPAR-γ activator, insulin sensitizer ADIPOSE

A

increased insulin sensitivity

98
Q

What do these do:

 α-Glucosidase inhibitors (Acarbos)- inhibits intestinal uptake of starch INTESTINE

A

decreased glucose absortion

99
Q

What does metformin do?

A

mimics exercise

100
Q

Cant you treat T1D with oral hypoglycemics?

A

no you need insulin injections or islet transplant

101
Q

Cant you treat T2D with oral hypoglycemics?

A

yes and insulin injections

102
Q

In the “basal” state, there is enough insulin to (blank) lipolysis, but it is a very low level. If there is another hormone around like epinephrine or cortisol, they win, and you have lipolysis.

After a meal, insulin increases to high levels. Under these conditions insulin wins and (blank) lipolysis, even if other hormones are present.

A

inhibit

turns off

103
Q

What does AMPK do in muscle?

A

stimulation of muscle glucose uptake and sitmulates insulin secretion

104
Q

What does G6Pase do?

A

it is the last step before getting glucose (i.e of gluconeogenesis or glycogenolysis) and it cleaves the phosphate off of G6P to make Glucose and it is THE ONLY way you can get glucose out of the liver

105
Q

If you have an issue with G6dehydrogenase what can results?

A

Hemolytic anemia

Block 3 Week 2 Dani (9 decks)

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