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GIGU > Endocrine cells of the pancreas > Flashcards

Endocrine cells of the pancreas Flashcards

1
Q

What do b cells secrete?

A

insulin and C peptide

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2
Q

What do alpha cells secrete?

A

Glucagon

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3
Q

What do delta cell secrete?

A

Somatostatin

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4
Q

What do F cells (PP cells) secrete?

A

Pancreatic polypeptide

Acts as a satiety signal

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5
Q

How does blood flow in the islets?

A

From center to periphery

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6
Q

How is insulin formed?

A

Preproinsulin –> proinsulin –> insulin and C peptide

Proinsulin still has C peptide attached

Proinsulin is packaged into secretory granules and then cleaved

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7
Q

What are the steps of insulin release?

A

Glucose enters cell via GLUT-2

Glucose is phyosphrylated by glucokinase

Glucose-6-phosphate is oxidized promoting ATP generation

ATP closes the “inward rectifying” K+ channels

Plasma membrane is depolarized and Ca2+ channels activate

Ca2+ enters cell and causes insulin and C-peptide to exocytosis

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8
Q

What closes the K+ channels?

A

ATP

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9
Q

What is the sulfonylurea receptor?

A

Increases insulin secretion by causing easier depolarization and more ca2+ entry

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10
Q

What are the intracellular steps of glucose uptake through GLUT4?

A

Insulin binds to receptor

physophorylation of insulin receptor substrate

Substrate proteins phosphorylate and activate/inactivate downstream pathways

Translocation of vesicles containing GLUT4 to membrane

Glucose enters via facilitated diffusion

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11
Q

What do MAP kinase, PI3k, and AKT do?

A

Increase glycogen/lipid/protein synthesis

decrease lipolysis

cell growth and differentiation

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12
Q

What does activation of AMP-kinase result in?

A

GLUT4 translocation to plasma membrane

this is indepedent of insulin

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13
Q

What are stimulatory factors of insulin secretion?

A

Increased glucose, AA, FA, and ketoacid concentration

Glucagon

Cortisol

GIP

K+

Vagal Stimulation, Ach

Sulfonylurea drugs

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14
Q

What are inhibitory factors of insulin secretion?

A

Decreased blood glucose

Fasting

Exercise

Somatostatin

alpha-adrenergic agonists; norepinephrine

Diazoxide (K+ channel activator, relaxes smooth muscle)-used to treat hypoglycemia

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15
Q

How does insulin affect skeletal muscle?

A

Increased glucose uptake

Increased glycogen synthesis

Incrased glycolysis and CHO oxidation

Increased protein synthesis

Decreased protein breakdown

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16
Q

How does insulin affect the liver?

A

Increases glycolysis and CHO oxidation

Decrease gluconeogensis

Increase pyruvate oxidation

Increase lipid storage and decrease lipid oxidation

17
Q

How does insulin affect adipose tissue?

A

Increased glucose uptake

Increased glycolysis

Decreased lipolysis

Promotes uptake of fatty acids

18
Q

How does insulin affect blood levels of certain substances?

A

The effect on blood level is the opposite of the action of insulin

Ex. Insulin increases protein synthesis so there are decreased AA in the blood

19
Q

Where is glucagon stored?

A

In dense granules of Alpha-cells

20
Q

What stimulates the secretion of glucagon?

A

Decreased blood glucose

Increased AA (arginine & alanine)

Fasting

CCK

B-adrenergic agonists

Ach

21
Q

What inhibits glucagon production and secretion?

A

Insulin

Somatostatin

FA

Ketoacids

22
Q

What are the affects of glucagon secretion?

A

Increased blood glucose

Increased glucoenogensis

Increased glucogenolysis

Inhibits glycogen synthesis

23
Q

Explain general diabetes for the blood

A

Insulin resistance –> decreased tissue glucose utilization –> spills over into blood –> hyperglycemia

24
Q

Explain general diabetes for adipose tissue

A

Increased lipolysis (free fatty acids) –> Polyphagia

Increased lipolysis–> gluconeogenesis and ketogenesis

25
Q

Explain diabetes for muscle

A

Increased protein catabolism (amino acids)

–> gluconeogenesis

26
Q

Explain general diabetes for liver

A

Glucagon excess leads to increased gluconeogenesis and Ketogenesis

27
Q

Explain general diabetes for the kidney

A

Ketoacidosis and hyperglycemia lead to ketonuria and glycosuria

–> polyuria–>volume depletion–> polydipsia

28
Q

What is type 1DM?

A

Destruction of B-cells

Decreased utilization of ketoacids results in diabetic ketoacidosis (DKA)

29
Q

What are some results of type 1 DM?

A

Hyperkalemia-shift of K+ out of cells

Increased blood glucose increased filtered load of glucose, exceeds reabsorptive capacity of proximal tubule

30
Q

What are some drawbacks of Type 1 DM insulin replacement?

A

Lag between glucose measurement & insulin dosing

delayed absoprtion of insulin following injections

31
Q

What is type 2 DM?

A

Exhaustion of active B-cells due to environmental factors

patients produce insulin but often have to produce more and more

32
Q

What are the results of obesity induced insulin resistance?

A

Decreased GLUT-4 uptake of glucose in response to insulin

Decreased ability of insulin to repress hepatic glucose production

Inability of insulin to repress adipose tissue uptake (LPL) and lipolysis (HSL)

33
Q

How else can Type 2 diabetes occur in non-obese patients?

A

Due to decreased insulin release by pancreas indepedent of peripheral insulin resistance

34
Q

What are incretin hormones and what do they do?

A

Hormones in the intestinne that are secreted in response to GI glucose and fat

Stimulates insulin secretion

Inhibits glucagon secretion

Slows gastric emptying

35
Q

What are some associated conditions of type 1 DM?

A

Autoimmune thyroid disease

celiac disease

addison’s disease

36
Q

What are some associated conditions to type 2 DM?

A

Obesity

lipid abnormalities

37
Q
A

GIGU (40 decks)

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