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Block 3; Week 2 > Mastick > Flashcards

Mastick Flashcards

1
Q

What is the problem in Type I Diabetes? What type of defect is it? What are the levels of insulin like? What is the treatment?

A

autoimmune destruction of beta cells
primary defect
there is no insulin!!
Treatment: insulin injections required or islet transplant

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2
Q

What is the problem in Type II Diabetes? What type of defect is it? What are the levels of insulin like? What is the treatment?

A

beta cell exhaustion–>compensation for insulin resistance
secondary defect
not enough insulin or maybe even high levels, but resistance
Treatment: oral hypoglycemia

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3
Q

What is the predicted transition in 2025 in terms of our issue w/ Diabetes?
What does this really mean?

A

Transition from diabetes epidemic to Diabetes tsunami…

this means that a higher percentage of the population is becoming diabetic…

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4
Q

What are some important complications of Diabetes?

A 
heart disease & stroke
hypertension
blindness
kidney disease
nervous system disease or neuropathy
amputations (non-traumatic)
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5
Q

T/F the pancreas is highly innervated (by parasymp & symp) & highly vascularized.

A

TRUE

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6
Q

What are the 2 main divisions of the pancreas?

A

Pancreatic Acini: secrete digestive juices into the duodenum

Islets of Langerhans: secrete insulin & glucagon into the blood

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7
Q

What separates the acini from the islets?

A

CT capsules

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8
Q

What are the 3 cells that make up the islets of Langerhans & what is their prevalence & what do they secrete?

A

Alpha cells; 25%; secrete glucagon
Beta cells; 60%; secrete insulin & amylin
Delta cells; 10%; secrete somatostatin

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9
Q

What are the functions of the following?
Insulin
Glucagon
Somatostatin

A

Insulin: anti-hyperglycemic (glucose clearance)
Glucagon: anti-hypoglycemic (glucose secretion)
Somatostatin: tonic modulator

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10
Q

What does it mean that somatostatin is a tonic modulator?

A

It means that glucose homeostasis could maybe be achieved w/o somatostatin…but it’s possible that larger & larger levels of insulin & glucagon would build up (in proper proportion). Somato keeps that from happening!! : )

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11
Q

What is the blood glucose level kept at in glucose homeostasis?

A

5.5mM

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12
Q

Glucagon, Insulin & somatostatin are all 3 ______ ______. They all begin in the ____ form. What does this mean?

A

3 peptide hormones
begin in the preproform.
The pre form means that you get across the ER & into the inside of a vesicle for secretion…

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13
Q

What is different about the way that proglucagon is broken up in intestinal cells?

A

The breakdown in intestinal cells releases incretins…

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14
Q

How does insulin begin? What is its status once it is at the vesicle?

A

Begins as preproinsulin. It is proinsulin by the time that it is secreted.

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15
Q

What are some important characteristics of proinsulin?

A

It has a C peptide as a part of it that is later cleaved…it is there to help with folding…
As far as secretion goes…C peptide & insulin are secreted in a 1:1 ratio…
However, C peptide isn’t degraded as quickly…so it can help indicate how much insulin has been secreted.

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16
Q

What is the relationship b/w the insulin, glucagon, & somatostatin in the human pancreas?

A

They work together & are all found intercalated & communicating.
Not as much the case in the mouse pancreas.

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17
Q

T/F The blood glucose levels remain relatively constant even during prolonged fasting or starvation.

A

TRUE.

even after 42 days of fasting!!

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18
Q

Describe the 4 phases of glucose homeostasis during fasting.

A 
Phase 1 (0-4hrs): well fed-->glucose from diet
Phase 2 (4-16hrs): post-absorptive-->glucose from glycogen stores in the liver & muscles
Phase 3 (2-7days): Early Gluconeogenic-->from gluconeogenesis
Phase 4 (7-42days): prolonged fasting or starvation-->from gluconeogenesis
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19
Q

According to the 4 phases of glucose homeostasis…when does the body start using ketones to supply the brain?

A

Phases 3 & 4

takes around 10-14 days

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20
Q

What are 2 ketone bodies that the body can use for fuel?

A

acetyl acetate

beta-hydroxybutyrate

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21
Q

T/F most of the time the blood sugar remains stable & doesn’t drop into hypoglycemia.

A

TRUE

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22
Q

What are some people groups that are at risk for hypoglycemia?

A

Diabetes patients w/ insulin but w/o food
People w/ insulin-producing tumors
Newborns w/ untreated galactosemia
Alcohol-poisoned people
People w/ liver diseases
Athletes who totally exceed their capacity.

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23
Q

What can happen progressively if you do experience hypoglycemia?

A

Faint
Coma
Death

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24
Q

What is considered the range that is normoglycemic?

A

4.5-8.

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25
Q

What is the oral glucose tolerance test?

A

It is a test for Diabetes. Patients are given a bunch of sugar & you observe their blood glucose levels to see if they get a sustained & crazy spike over 200mg/dL.
Shows if that insulin is working…

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26
Q

What happens to a patient in the case of hyperglycemia?

A 
nothing really at first, but with chronic exposure the following can happen:
Blindness
Kidney Disease
Nervous System Disease (neuropathy)
Amputation
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27
Q

What do glucagon & insulin typically do in response to a meal?

A

Insulin will increase dramatically.
The glucagon will probably only decrease slightly, if at all…it is relatively constant.
The insulin/glucagon ratio does change, however. You should think in terms of that! : )

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28
Q

What does a high protein meal do to insulin & glucagon?

A

It significantly increases both insulin & glucagon.

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29
Q

What does glucagon do between meals?

A

Glucagon stimulates the liver to release glucose (glycogenolysis) & keeps the blood glucose around 4.5.

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30
Q

T/F Glucagon receptors are found in the muscle, liver, & adipose tissue.

A

FALSE.

Glucagon receptors are only found in the liver.

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31
Q

What happens first…glycogenolysis or gluconeogenesis?

A

Glycogenolysis

32
Q

During an overnight fast, what happens to the following:
glycogen synthesis
lipolysis
lipogenesis

A

Glycogen synthesis is inhibited.
Lipolysis is stimulated.
Lipogenesis is inhibited.

33
Q

If glycogen synthesis in muscle tissues is inhibited…what does that do to the amount of glucose required from the blood?

A

It decreases it. The muscles don’t need their glucose supplied by the blood.

34
Q

During fasting, what happens to the resting glucose transport?

A

It is decreased 3-4 fold relative to the fed (insulin high) state.

35
Q

Even if your insulin isn’t high or your insulin isn’t helping you (Type II D)…what is another way to accomplish glucose uptake by tissues?

A

Glucose uptake can be stimulated by exercise. When exercising & muscles use up their glycogen…AMP increases & activates the AMPKinase. This can then accomplish more glucose uptake.

36
Q

Glucose transport into adipocytes is very low/high in basal adipocytes.

A

VERY LOW

37
Q

T/F It takes a LOT of insulin to inhibit the breakdown of fat in adipose tissues.

A

FALSE It doesn’t take much insulin to inhibit the breakdown of fat.

38
Q

After a meal…the blood glucose increases & insulin is released. What are the 3 main target tissues for insulin where it increases glucose transport? What is the main target?

A

Liver
Fat
Muscle***most of it goes here!!

39
Q

What happens in a fed metabolic state in the liver?

A

glycogenolysis inhibited
gluconeogenesis inhibited
lipolysis inhibited
glycogen synthesis stimulated

40
Q

What happens in a fed metabolic state in the muscles?

A

The rate limiting & important step for Diabetes patients (glucose transport increases 4 fold).
Glycogen synthesis stimulated
Glycogenolysis inhibited

41
Q

T/F Lipogenesis is rate limited by glucose transport into adipocytes.

A

True.

42
Q

T/F Low insulin levels increases glucose transport 20-50 fold in adipocytes.

A

FALSE

High insulin levels…

43
Q

When you exercise…what happens in terms of the muscle & AMPK?

A

Muscle needs more glucose & uses up its glycogen stores. AMPK activated.
Then it increases its glucose uptake.
This decreases the blood glucose levels.
Glucagon relatively increases & insulin decreases.

44
Q

When glucagon is dominating & there is movement toward free glucose…which enzyme is activated? What is the phosphorylation situation?

A

PKA is activated
The enzymes that break down are phosphorylated & activated.
The enzymes that build up are phosphorylated & deactivated.

45
Q

When insulin is dominating & there is movement toward stored glucose…which enzyme is activated? What is the phosphorylation situation?

A

PP1
The enzymes that build up are dephosphorylated & activated.
The enzymes that break down are dephosphorylated & inactivated.

46
Q

How does glucose enter a cell?

A

Thru GLUT transporters. These are bidirectional pores. They just allow glucose to flow down its concentration gradient.

47
Q

What happens as soon as glucose is transported into the cell?

A

It is phosphorylated & trapped. (by either hexokinase or glucokinase).
This means that there is no free glucose lying around the cell.
Glucose-6-phosphate can’t exit thru the GLUT transporters.

48
Q

What is something special about the liver that is different than other cells? In terms of trapping glucose…

A

Well…normally G-6-P can’t get thru GLUT. But in the liver there is also Glucose-6-Phosphatase present, so that it can remove the extra phosphate & allow it to get back thru the transporter.
This is done during periods of fasting.

49
Q

Which direction does glucose flow thru the GLUT transporter?

A

Down the conc’n gradient of glucose. If blood glucose under 4mmol/L–>it flows into the cell.

50
Q

Which organ expresses the GLUT transporters with the highest affinity? Why is this important?

A

THE BRAIN! B/c the brain needs delivery of a constant amount of glucose.
Has:
Glut 3: highest affinity–>Km=0.4mM

51
Q

Which organs/cells express GLUT transporters with a low affinity?

A

Liver
Intestine
Pancreatic Beta Cells
**Glut 2; Low Affinity: Km=15mM

52
Q

Which organs express GLUT transporters with relatively high affinity? Glut 4

A

Heart
Skeletal Muscle
Fat
**Glut 4: High affinity; insulin-regulated; Km=1mM

53
Q

Which organs express GLUT transporters with relatively high affinity? Glut 1

A

Pancreatic Alpha cells
most other tissues
**Glut 1: High affinity, Km=1mM

54
Q

Explain the process of insulin secretion in pancreatic beta cells.

A

Glucose enters the Glut 2 transporter (low affinity) of pancreatic beta cells.
The glucose is immediately phosphorylated by glucokinase into G6P & trapped in the cell. It goes thru glycolysis & respiration & increases the ratio of ATP/ADP inside the cell.
The extra ATP inhibits the potassium channel from allowing K+ to exit the cell. The increase in positive charge causes a depolarization that reaches the voltage-gated calcium channel & allows for an influx of Ca++…This stimulates the release of insulin packaged in its safe little vesicles. Enjoy the journey vesicle!

55
Q

What is one of the advantages of beta cells having low affinity & high capacity Glut 2 transporters & phosphorylating enzymes?

A

B/c of this a small change in glucose causes a significant change in ATP/ADP ratio & insulin secretions…

56
Q

What is the significance of alpha cells having a high affinity?

A

This means that with normal levels of glucose, there is no change in glucose transport & no changes sensed.

57
Q

T/F There are many ways to control glucagon secretion.

A

TRUE.

58
Q

What is the main way of controlling glucagon secretion?

A

thru the levels of insulin…

59
Q

What’s the deal with glucose transport in muscle & fat?

A

It is regulated by insulin. It expresses Glut 4 which is high affinity & low capacity.
The glucose transport is rate limited by the total number of transporters inserted into the plasma membrane.

60
Q

How much does insulin increase glucose transport in fat? in muscle?

A

Fat: 20-50 fold
Muscle: 3-4 fold
**Muscle can also get glucose transport thru exercise & AMPK.

61
Q

What is released from the pancreas & is considered a tonic modulator? What cell is it released from?

A

Somatostatin

delta cells

62
Q

What are 2 plans of attack that work on beta cells to increase their insulin secretion?

A

Sulfonylureas will increase their secretion by acting on K+ channels directly, inhibiting them.
This causes depolarization, opens the voltage-gated calcium channels & allows the vesicles to flee.
Incretins in the intestines bind to the receptors on the beta cell & make it more suspectible to the insulin.

63
Q

Which of the following is considered a secretagogue? Sulfonylurea or incretins?

A

Sulfonylureas.

All secretagogues act directly on the K+ channel.

64
Q

What do DPP-4 inhibitors do?

A

They increase insulin secretion by slowing incretin turnover.

65
Q

What are 4 things that can increase insulin secretion?

A

Sulfonylurea
Other secretagogues
Incretin analogues
DPP-4 inhibitors

66
Q

What are 2 things that can increase insulin sensitivity?

A

Biguanides (Metformin)

Thiazolidinediones (Avandia)

67
Q

What do biguanides or metformin do? What tissue type do they target?

A

They activate AMPK. It is an insulin sensitizer. It sort of mimics exercise. It acts on muscle.

68
Q

What do thiazolidinediones (Avandia) do? What tissue type do they target?

A

They are PPAR gamma activators. They are insulin sensitizers. They act on adipose. These are the ones Mastick developed.

69
Q

What is something that could decrease glucose absorption?

A

alpha glucosidase inhibitor (Acarbos)
This inhibits intestinal uptake of starch.
It acts on the intestines.

70
Q

Why might sulfonylureas not be a good choice for a late stage Type II Diabetes patient?

A

Beta cell burnout

It might not be a good idea to stimulate the cell to secrete more insulin when it is already suffering.

71
Q

What are the 3 possible ways that oral hypoglycemics can work?

A

Increasing insulin secretion
Increasing insulin sensitivity
Decreasing glucose absorption

72
Q

What is an injected hypoglycemic?

A

a bunch of things that look like insulin/act llke insulin.

73
Q

What are the treatment options for Type I Diabetes?

A

insulin injections or islet transplants–>NOT oral hypoglycemics.
Remember: the beta cells were destroyed (autoimmune)

74
Q

What are the treatment options for Type II Diabetes?

A

oral hypoglycemics
if the patient is late stage–>insulin injections
**Remember: these patients are experiencing beta cell burnout.

75
Q

What does a defect in G6P dehydrogenase do?

A

decreases NADPH & the ability to reduce glutathione

76
Q

Alcoholics are usu deficient in what? This means that which enzyme can’t function? What is the result?

A

Deficient in thiamine
Pyruvate Dehydrogenase can’t function
Lactic acidosis & lethargy results…

Block 3; Week 2 (9 decks)

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