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Endocrinology > Lecture 9: Pancreas > Flashcards

Lecture 9: Pancreas Flashcards

1
Q

The exocrine cells of the pancreas are

A

acinar and duct

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2
Q

beta cells make and secrete __________

A

insulin

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3
Q

glucagon is made by ________

A

alpha cells

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4
Q

Somatostatin is made by _________

A

delta cells

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5
Q

What do PP cells make?

A

pancreatic polypeptide (inhibit acinar cells)

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6
Q

What are the 2 major pancreatic hormones?

A

1) Insulin (anabolic)

2) Glucagon (catabolic)

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7
Q

What are the 4 minor pancreatic hormones?

A

1) somatostatin
2) amylin
3) pancreatic polypeptide
4) ghrelin

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8
Q

How many islets does the human pancreas have?

A

1 million

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9
Q

What kind of capillaries populate the pancreas?

A

fenestrated

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10
Q

Beta cells are clustered in the _______ while other cells are in the _________

A

core (surrounded by alpha cells); mantle (near vasculature)

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11
Q

True or false: glucagon has a direct effect on the beta cell to influence insulin

A

FALSE (paracrine effects only)

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12
Q

How does blood flow to the islet?

A

arteriole projects into center of islet, insulin rich blood flows from center to periphery of islet

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13
Q

What is the half life of insulin?

A

3-8 mins (VERY short)

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14
Q

What is the half life of C-peptide?

A

35 mins (used as indicator of pancreatic function)

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15
Q

Why is the cleavage of C peptide so critical?

A

exposes end of insulin chain that interacts with receptor

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16
Q

What peptides make up insulin?

A

A and B chains

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17
Q

What is the first step in insulin release?

A

1) glucose outside the beta cell stimulates insulin production

GLUT-2 receptor senses high glucose (has low affinity for glucose so only detects high conc. allowing glucose into the cell)

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18
Q

Once glucose enters the beta cell, what happens?

A

glucokinase phosphorylates glucose which traps it into the cell

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19
Q

What is the pancreatic glucose sensor?

A

glucokinase (not activated unless glucose is high)

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20
Q

What is the second step in insulin release?

A

2) glucose inside beta cell (glucose is phosphorylated by glucokinase —— G6P generates ATP)

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21
Q

What is the third step of insulin release?

A

3) glucose metabolism

increased ATP closes K+ channels (as do sulfonylurea drugs since K+ channels have a SUR subunit)

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22
Q

How do sulfonylurea drugs work and what are they used for?

A

close the potassium channels (used as the earliest antidiabetic drugs) and bypass glucose step

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23
Q

What is the benefit to the K+ channels closing?

A

holds more K+ inside the cell causing it to depolarize (influx of sodium into the cell)

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24
Q

What is the 4th step in insulin release?

A

cell depolarization

closing K+ channels depolarize cell which opens the Ca++ channels

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25
Q

What happens after Ca++ channels open/the cell is depolarized?

A

5) vesicle exocytosis

Ca++ influx causes exocytosis of insulin-containing vesicles

26
Q

Go over the steps of insulin release once more

A

1) high glucose outside beta cell (GLUT-2)
2) Glucose inside beta cell (G6P via glucokinase)
3) Glucose metabolism (makes lots of ATP)
4) Cell depolarization (activates Ca++ channels)
5) Vesicle exocytosis (insulin)

27
Q

What are 3 modulatory pathways to promote insulin release?

A

1) FFAs, Amino Acids (both increase ATP)
2) Incretins (GLP-1) potentiate insulin release but still needs glucose
3) catecholamines (inhibit release via alpha-adrenergic receptors)

28
Q

Why is insulin release biphasic in response to glucose?

A

5% of vesicles are available for immediate release (docked at membrane)

95% are “stored” or reflect newly synthesized insulin

29
Q

Diabetic patients usually lack which phase of insulin release?

A

first phase (fewer vesicles docked at membrane)

second phase is a flat line

30
Q

What kind of receptors are insulin receptors?

A

RTKs (insulin binds alpha subunit and then beta subunit is autophosphorylated)

31
Q

Where are the 2 sites of greatest insulin stimulated glucose uptake?

A

muscle and fat

32
Q

Once insulin binds to RTKs and they are autophosphorylated, what happens inside the muscle cell?

A

phosphorylated receptor recruits IRSs (insulin receptor substrates) which activate intracellular signaling cascades

33
Q

What is the end result of insulin binding on a muscle cell?

A

insertion of GLUT-4 so that glucose can enter the cell

34
Q

What are the 2 downstream pathways for insulin substrate?

A

1) MAPK (recruits docking proteins which activate MAPK effecting growth and mitogenic effects)
2) PKB (causes GLUT4 to be inserted into the membrane)

35
Q

Metabolic effects of insulin are mediated through __________ which mitogenic effects are mediated through __________

A

Metabolic: PKB (get GLUT4 on the membrane)

Mitogenic: MAPK

36
Q

What is the ONLY insulin dependent transporter?

A

GLUT4 (skeletal muscle, fat; stored inside cell under basal conditions)

37
Q

What is the glucose transporter used in the brain?

A

GLUT3

38
Q

Where is GLUT2 expressed?

A

pancreatic beta cells, liver, intestine, kidney

39
Q

What is the glucose transporter for brain vasculature?

A

GLUT-1

40
Q

What are the effects of insulin on the liver?

A

promote glycogen and TG production — can get too much TG synthesis/fatty liver (stimulates glucokinase)

reduces glucose production/output (inhibits G6 phosphatase)

41
Q

What are the effects of insulin in the muscle?

A

promotes glycogen and TG production, protein synthesis

42
Q

What are the effects of insulin on fat?

A

promotes TG production, release FFAs from chylomicrons, glycolysis

inhibits lipolysis

43
Q

Overall, net effect of insulin is __________

A

anabolic! builds things to store energy, not breaks them down

44
Q

What are incretins?

A

GLP-1 and GLP-2

GLP-1 responds to carbs and travels to pancreas to potentiate release of insulin

45
Q

What do incretins do?

A

target beta cells to stimulate more hormone production

46
Q

how are incretins related to glucagon?

A

synthesized from the same prohormone

have tissue specific enzymatic activity

47
Q

Name 2 things that stimulate glucagon release

A

1) Amino acids (protein meals)
2) catecholamines (exercise)

BOTH WANT TO MOBILIZE ENERGY

48
Q

What are the main targets of glucagon?

A

liver and adipose

49
Q

True or false: there are no glucagon receptors in skeletal muscle

A

TRUE

50
Q

How does insulin affect ketogenesis?

A

INHIBITS IT (which is why diabetics have ketoacidosis - no insulin to stop producing ketones)

51
Q

Why dont type 2 diabetics experience ketoacidosis?

A

insulin is still present

52
Q

True or false: insulin and glucagon target the same enzymes but have different functions

A

TRUE

insulin: dephosphorylate to turn enzyme into kinase pushing metabolic pathway towards glycolysis
glucagon: phosphatase activity

53
Q

What does somatostatin do?

A

suppresses insulin release (and is inhibited by insulin) stimulated by high fat, high carbs like insulin

54
Q

What does amylin do?

A

contributes to beta cell destruction? released with insulin in vesicles from beta cells

55
Q

What can be used to treat insulin producing tumors?

A

somatostatin (blocks insulin release)

56
Q

What does ghrelin do?

A

inhibits insulin release (G activation of K+ channels)

decreases intracellular Ca++ to decrease insulin release

57
Q

Where is Ghrelin made? and when?

A

stomach (responds to lack of food/stretch to stimulate eating)

58
Q

What are insulin counter regulatory hormones?

A

1) Glucagon
2) Growth hormone/cortisol
3) Catecholamines (epi) – raises plasma glucose levels during exercise

59
Q

When insulin is present, what happens to GH levels?

A

increase! AA from protein stimulates GH which stimulates IGF-1

GH opposes insulin lipogenesis

60
Q

True or false: insulin directly affects glucagon but not the other way around

A

TRUE (due to blood flow)

Endocrinology (16 decks)

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