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Physiology Block 3- Endocrine Physiology > L6 - Endocrine Pancreas > Flashcards

L6 - Endocrine Pancreas Flashcards

1
Q

Approximately what percent of the pancreas is composed of Islets of Langerhans?

A

10%

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2
Q

What is secreted by the cells of the Islets of Langerhans?

A

Alpha secrete glucagon, beta secrete insulin, and delta secrete somatostatin

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3
Q

What is the structure of insulin? How is it synthesized?

A

Composed of two chains (alpha and beta) connected by disulfide bridges; Proinsulin is posttranslationally cleaved into insulin and clear (c-) peptide

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4
Q

How is insulin released? What causes this pattern?

A

Biphasic, pulsitile pattern of release: there is an initial large peak of release due to readily releasable granules, followed by a prolonged, but less powerful release of granules that take tome to mature, prime, and mobilize

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5
Q

What is the ratio of insulin to clear peptide released from the beta cell?

A

1 : 1

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6
Q

What is the physiologic importance of a pulsitile release of insulin?

A

Important for achieving the maximal physiologic effects– esp.in the suppression of liver glucose production, and in insulin-mediated glucose utilization by adipose and muscle

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7
Q

When is insulin release highest?

A

Post-prandially

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8
Q

How does insulin circulate? What is the half-life?

A

Circulates free- half-life of 3-8 minutes

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9
Q

How much of the insulin released by the pancreas is metabolized by the liver on its first pass through?

A

About 50%

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10
Q

What is the best index of pancreatic secretory function? Why?

A

C-peptide because it is more resistant to degradation than insulin

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11
Q

What is the normal pathway of insulin release?

A

Glucose enters the cell through GLUT2 transporter and enters glycolysis, TCA, making ATP. The increased ATP/ADP ratio inhibits the ATP-sensitive potassium channel on the membrane, resulting in depolarization of the cell, opening voltage gated calcium channels allowing Ca++ influx which is necessary to mobilize insulin containing granules so they can release contents

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12
Q

What compounds can stimulate/ potentiate insulin release? Inhibit?

A

Amino acids, ketoacids, ACh, cholecystokinin, glucagon, and glucagon-like peptide; Epi, NE, and somatostatin all inhibit insulin release

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13
Q

What is a sulfonylurea receptor? What is the effect of sulfonylurea on insulin release?

A

ATP-sensitive K+ channel; Stimulation of release

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14
Q

What is the relationship between K+ current and ATP levels?

A

Increasing concentrations of ATP will slowly decrease the K+ current

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15
Q

What is the structure of the insulin receptor? How does binding mediate cellular change?

A

Two chains outside and two chains inside the cell; Binding recruits insulin receptor substrates (IRS1-4)

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16
Q

What are the effects of insulin binding?

A

Increased glucose uptake, glycolysis, glycogen synthesis, and decreased gluconeogenesis decrease plasma glucose; Increased lipogenesis and decreased lipolysis favors buildup of adipose; Stimulation of protein synthesis and decreased proteolysis favors buildup of muscle

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17
Q

What happens to insulin-receptor complex following binding?

A

The complex is internalized, the hormone is degraded and the receptor is recycled to membrane

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18
Q

How is insulin receptor expression modulated?

A

With high concentrations of insulin, excess growth hormone, or obesity, there is a decrease in insulin receptor expression. With exercise or fasting/starving, there is enhanced insulin receptor expression

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19
Q

What are the early effects of insulin on the cell (Esp. adipocytes and muscle cells)?

A

Increases expression of GLUT4 on the plasma membrane; it can also increase influx of K+, activate the Na+/H+ antiporter, which increases Na+ into the cell resulting in increased Na+/K+ ATPase activity, pumping Na+ out to bring K+ in

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20
Q

Which of the glucose transporters are insulin-sensitive?

A

GLUT4

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21
Q

True or False: The brain requires insulin to bring glucose into the cell?

A

False

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22
Q

What is the major neuronal glucose transporter?

A

GLUT3

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23
Q

Which glucose transporter can transport fructose? Where is it found?

A

GLUT5 in sperm and small intestines

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24
Q

What is the overall effect of insulin on hepatic glucose output?

A

Decreases

25
Q

What would result from sustained insulin stimulatino?

A

The prolonged exposure to insulin would activate the MAP kinase pathway which is linked with proliferative responses, leading to vascular smooth muscle cell proliferation. This can lead to hypertension and cardiovascular disease

26
Q

What is the net effect of insulin on blood glucose levels?

A

Decreased (restored) levels

27
Q

In what tissues is proglucagon expressed?

A

Brain, alpha pancreas cells, and intestine

28
Q

What products can be derived from proglucagon? In what tissues?

A

Glucagon (pancreas alpha cells) and glucagon-like peptide 1 (intestines)

29
Q

What are the half lives of glucagon and GLP-1? What is the reason for the difference?

A

Glucagon is 5-10 minutes, and GLP-1 is less than 2 minutes becasue of dipeptidyl-piptidase IV

30
Q

What stimulates glucagon release? What inhibits its release?

A

Hypoglycemia, epinephrine binding to B2, vagal stimulation; Hyperglycemia and somatostatin

31
Q

Why does it make sense for glucagon release to be stimulated by both vagal activity and epinephrine?

A

Vagus is parasympathetic which is active during eating, so when blood glucose is going up, and so it protects from hypoglycemia; Epinephrine stimulation will help maintain plasma glucose so it can be drawn upon for fuel in the “fight-or-flight” response

32
Q

What signaling cascade is stimulated by binding of Glucagon to its receptor? What is the overall effect?

A

Binding to GsPCR–> increased cAMP–> activated PKA; overal effect is to increase hepatic glucose output

33
Q

What are the physiologic effects of glucagon at its target organs? How does it act in cases of stress or food deprivation?

A

Increases hepatic glucose output by increasing glycogenolysis and gluconeogenesis, and by decreasing glycolysis; Under conditions of stress and starvation, it increases activity of hormone-sensitive lipase, leading to lipolysis and release of glycerol and FFA

34
Q

What are incretins?

A

Molecules that favor or facilitate insulin release

35
Q

What are the effects of glucagon-like peptide 1?

A

Amplification of glucose-induced insulin release, decreased gastric emptying, decreased appetite, decreased glucagon secretion and increased beta cell proliferation

36
Q

True or False: Overstimulation by GLP-1 is likely to lead to hypoglycemia?

A

False- only helps make more insulin in response to hyperglycemia

37
Q

Why is DPP4 a good pharmaceutical target?

A

Inhibition of DPP4 will keep GLP-1 around longer, which will amplify insulin release and suppress glucagon release

38
Q

What is the half-life of somatostatin? When is it released?

A

1-3 minutes; released following a meal

39
Q

What are the effects of somatostatin?

A

Decrease GI and pancreatic exocrine and endocrine function and decrease cell proliferation

40
Q

When is pancreatic polypeptide released? What are its effects?

A

Released following a meal, exercise, or vagal stimulation; thought to modulate pancreatic and GI exocrine secretion and have an effect on feeding behavior

41
Q

What cells secrete amylin? What are its effects?

A

Beta pancreas cells; suppresses glucagon expression and decreases gastric emptying

42
Q

How does Type I and II diabetes affect amylin secretion?

A

Type I diabetics have no beta cell function and so there is no amylin secretion. In type II diabetics, there is amylin secretion but no changes in response to a meal

43
Q

Why does it make sense to use amylin as an adjunct treatment to be used with insulin in diabetics?

A

It suppresses post-prandial glucagon release, lowering hepatic glucose production and maintaining lower glucose blood levels

44
Q

What are alternate names for Type I diabetes? Type II? Which is more common?

A

Insulin-dependent diabetes mellitus or juvenile onset diabtes; Non-insulin dependent or adult-onset diabetes; Type II is 90-95 percent of cases

45
Q

What results in Type I diabetes? What is it characterized by?

A

Destruction of beta pancreas cells; ketoacidosis in the absence of insulin therapy

46
Q

What are the risk factors for Type II diabetes?

A

Age, obesity, Family Hx, Gestational diabetes, impaired glucose tolerance, sedentary life, hispanic or african american ethnicity

47
Q

What characterizes Type II diabetes?

A

Milder hyperglycemia and rare ketoacidosis

48
Q

What is the pathophysiology of Type II diabetes?

A

There is a decreased response to insulin resulting in higher hepatic glucose production and decreased glucose uptake by skeletal muscle and adipose all contributing to hyperglycemia

49
Q

What is the earliest physiologic indication of beta cell dysfunction? How does hyperinsulinemia and insulin resistance result?

A

Delayed and sluggish and lower insulin response to glucose post meal, increasing fasting glucose; the pancreas increases insulin secretion in response to hyperglycemia which ultimately downregulates insulin receptors resulting in decreased insulin sensitivity

50
Q

What are the characteristic manifestations of diabetes?

A

Polyphagia, polyuria, and polydipsia

51
Q

What are the criteria for diagnosing diabetes mellitus? Which is the gold standard?

A

Symptoms of diabetes plus a random blood glucose of greater than 200 mg/dl OR fasting plasma glucose of 126 mg/dL or more OR 6.5% or greater HbA1c (gold standard) OR 2 hr plasma glucose > 200 mg/dL during an oral glucose tolerance test

52
Q

What are the potential consequences of chronically high HbA1c levels?

A

There is an increased rate of heart problems/ failure and death

53
Q

How does diabetic ketoacidosis result?

A

Stressful stimuli stimulate hormone sensitive lipase to degrade TAG into glycerol and FFA. Ketone bodies form and effect acid-base balance resulting in acidosis

54
Q

What is hyperglycemic hyperosmolar nonketotic Syndrome?

A

A complication of type II diabetes in which lots of glucose increases osmolarity but there is no synthesis of ketone bodies

55
Q

How does insulin-induced hypoglycemia result in diabetes?

A

Excess insulin in the blood will push glucose into tissues, stimulate glucagon release and allow glycogen breakdown to occur unopposed in skeletal muscle and result in release of GH and cortisol

56
Q

What are the vascular and non-vascular chronic complications of diabetes?

A

Microvascular- retinopathy, neuropathy, nephropathy; macrovascular- coronary heart, peripheral arterial and cerebrovascular disease; nonvascular- gastroparesis, infections, hearing loss, skin changes

57
Q

(L6) Sulfonylureas result in:

a) decreased beta cell insulin release
b) increased beta cell ATP production
c) increased beta cell insulin release
d) decreased beta cell ATP production

A

c) increased beta cell insulin release

sulfonylurea blocks K+ efflux channel, increasing the depolarization of the cell membrane, activating Ca2+ influx of the cell => releasing insulin cells

*will not work with TYPE 1 diabetes because they do not have beta cells

58
Q

(L6) Insulin release from the beta cell ______

a) decreases as [ATP] increases
b) increases as [ATP] levels decrease
c) increases as K+ efflux drops
d) decreases as K+ efflux drops

A

c) increases as K+ efflux drops

when K+ is retained in the cell, the membrane potential increases activating Ca2+ channels to open, increasing the influx of Ca2+ to enter the cell => release of insulin

Physiology Block 3- Endocrine Physiology (10 decks)

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