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ENRE > Endocrine Pancreas > Flashcards

Endocrine Pancreas Flashcards

1
Q

What are the endocrine cells in the pancreas and what do they secrete?

A

alpha = glucagon

beta = insulin, C peptide

delta = somatostatin

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2
Q

How are the endocrine cells arranged in islets?

A

betas in the center

alpha and delta in the periphery

(alpha and delta get bathed in insulin)

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3
Q

What does sympathetic stimulation do to the pancreas?

Parasympathetic?

A

alpha adrenergic signal –> decreased insulin

ACh –> increased insulin

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4
Q

How do cells of pancreatic islets communicate with each other?

A

gap jxns = rapid cell-to-cell communication btw a-a, a-b, b-b

blood flows into center of islets first –> goes out = all cells get bathed in insulin

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5
Q

How do delta cells affect beta and alpha cells?

A

somatostatin inhibits insulin and glucacon secretion

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6
Q

How do beta cells affect alpha and delta cells?

A

beta cells inhibit alpha cells

alpha cells promote insulin

delta cells inhibit beta cells

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7
Q

How are the alpha and beta strands of insulin held together?

A

by 2 disulfide bridges

C peptide initially holds them together but is then cleaved to form the active hormone

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8
Q

What is the main stimulus for insulin?

A

carbohydrate or protein-containing meal –> high glucose levels

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9
Q

What is the difference between preproinsulin, proinsulin, and insulin?

A

preproinsulin = signal peptide, A and B chains, and connecting peptide

proinsulin = no signal peptide; C peptide, disulfide bridges form in ER –> packaged in vesicles in golgi

during packaging, proteases cleave proinsulin

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10
Q

What is the importance of C peptide?

A

insulin and C peptide are packed together in secretory vesicles –> secreted in 1:1 ration

C peptide can be used as long-term marker of Beta cell function and insulin secretion

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11
Q

How does glucose signal insulin release?

A

glucose binds glut2 – glucokinase –> G-6-P –> makes ATP –> closes K+ channels –> cell depolarizes –> voltage-gated Ca channels open –> exocytosis of insulin and C peptide

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12
Q

What do sulfonurea drugs do?

A

promote the closing of ATP-dependent K+ channels (glucose signals this) –> so that more insulin will be secreted

used to treat T2DM

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13
Q

How is insulin secreated in response to glucose?

A

biphasic manner

phase 1 = preformed vesicles released

phase 2 = preformed and newly synthesized insulin released

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14
Q

In diabetic ppl, what is the first thing to disappear?

A

the first phase/ acute insulin response

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15
Q

How do CCK and ACh contribute to insulin release?

A

both bind Gq receptor –> PLC –> IP3 and DAG –> both calcium and PkC signal insulin release

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16
Q

How does somatostatin contribute to insulin release?

A

binds Gi –> inhibits cAMP and PkA –> inhibits insulin release

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17
Q

How do glucagon and GLP-1 contribute to insulin release?

A

Binds Gs receptor –> cAMP –> PkA –> insulin release triggered

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18
Q

What happens (in general) when insulin binds its receptor?

A

receptor phosphorylates itself and other proteins –> insulin-receptor complex is internalized by target cell –> glucose transport, protein, fat, and glycogen synthesis; growth and gene expression

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19
Q

How does insulin affect its own receptor?

A

down regulates its own receptor

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20
Q

What is the relationship btw insulin and the liver?

A

insulin released from pancreas –> to liver, can take up insulin and receptor and cleave –> actual levels in systemic circulation are a lot less than what is initially released from the pancreas

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21
Q

What receptors do insulin upregulate in cell membranes?

A

GLUT4 in muscle and adipose tissue

GLUT2 in liver

other GLUTs

22
Q

How does insulin induce metabolic effects?

A

binds receptor –> Piates –> IRS1-4 –> PI3K –> PIP3 –> pkB/AKT –> metabolic effects

*include GLUT translocation and activation of protein postphatases

23
Q

How does insulin induce growth effects?

A

insulin + receptor –> Piates –> IRS1-4 –> SHC –> GRB/SOS –> RAS/GTP –> MAPK –> growth effects

24
Q

How does insulin affect glycogen?

A

increases glucogen synthase

upregulates hexokinase (glucokinase in liver and beta cells)

activates glycogen synthase

25
Q

How does insulin affect protein and fat metabolism?

A

increases protein synthesis and decreases protein breakdown

favors FAs –> triglycerides (lipogenesis)

inhibits triglycerides –> FAs by inhibiting hormone-sensitive lipase

26
Q

How does excercise affect insulin and glucose metabolism?

A

muscle contractions stimulate AMPK –> GLUT4 into membranes –> helps uptake of glucose and decreases insulin resistance

27
Q

How does insulin affect blood levels of nutrients?

A

decreases:

glucose, FAs, ketoacids, amino acids

(basically puts it all in cells)

28
Q

How does insulin affect K+ levels?

A

increases K+ uptake into cells and lowers plasma K

glucose and insulin can be given to treat hyperkalemia

29
Q

When do symptoms of T1DM become evident?

A

not until 80% of beta cells are destroyed

30
Q

What occurs to induce diabetic ketoacidosis?

A

increased conversion of FA to ketoacids and decreased ketoacid utilization by tissues

31
Q

What things do you see increased in the blood in T1DM?

A

glucose

fatty acids and ketoacids

amino acids

K+ (even though total body K is usually low)

32
Q

What occurs to induce hyperkalemia in type 1 diabetics?

A

insulin doesn’t have effect on Na/K ATPase –> K shifts out of cells –> plasma levels become high, but total is usually low bc of polyuria and dehydration

33
Q

What occurs in osmotic diuresis?

A

increased blood glucose –> increased filtered load of glucose, exceeding reabsorptive capacity of PCT

water and electrolyte reabsorption is also prevented

Polyuria: increased excretion of Na and K even though urine concentration of electrolytes is low

34
Q

What are the main drawbacks of insulin replacement therapy?

A

lag btw glucose measurement and insulin dosing, delayed absorption of insulin following injection –> periods of hyperglycemia

35
Q

What occurs in the progression of T2DM?

A

initially high insulin levels and insulin resistance –> progressive exhaustion of beta cells –> insulin deficiency later

36
Q

What are teh 3 causes for 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 hormone-sensitive lipase (HSL) or increase lipoprotein lipase (LPL)

37
Q

What is the current understanding of insulin resistance?

A

not well understood

might be due to post-receptor signaling –> ultimately results in less gluts in membranes

*may be bc insulin receptor or downstream proteins aren’t Piated

38
Q

What do biguanide drugs do?

A

upregulate insulin receptors on target tissues

(metformin)

39
Q

What is the difference in effects of IV glucose vs oral glucose?

A

insulin is much more affected by oral glucose than IV

40
Q

What are incretin hormones and what do they do?

A

intestine-derived, short T1/2

GLP-1, GIP

GI glucose and fat –> stimulate insulin secretion, inhibit glucagon, slow gastric emptying

41
Q

What is the reduced incretin effect?

A

in type 2 diabetics, oral glucose fails to result a mich higher peak of insulin that is seen in normal ppl

bc incretins aren’t working to increase insulin

42
Q

Which form of diabetes has more of a genetic component?

A

type 2 = 50% family link rather than 10-20 for type 1

43
Q

What hormones have a hyperglycemic action?

A

glucagon

epinephrine

cortisol

growth hormone

44
Q

What other hormones are part of the same family as glucagon?

How do they differ?

A

GLPs are in same family

proglucagon –> processing in alpha cells –> glucagon

proglucagon –> processing in intestinal L cells –> GLP-1 and GLP-2

45
Q

How is glucagon stored?

A

in dense granules until alpha cells are stimulated

46
Q

What is the main stimulus for glucagon secretion? How does it work?

A

low glucose

no glut signaling –> increased ATP –> K channel inhibited, Na and Ca channels open –> Ca stimulates glucagon release

47
Q

Besides low glucose, what other things stimulate glucagon release?

A

amino acids

fasting

CCK

beta adrenergic agonists

ACh

48
Q

What things inhibit glucagon synthesis and secretion?

A

insulin

somatostatin

increased FA and ketoacid concentration

49
Q

What are the major actions of glucagon?

A

increases glycogen breakdown

Glucagon –> cAMP –> PKA –> inhibits production of fructose 2,6-biPi –> substrates directed toward glucose formation

50
Q

How does glucagon affect lipid metabolism?

A

increases lipolysis and inhibits FA synthesis

shunts substrates toward gluconeogenesis

increased blood glucose, FAs, and ketoacids

51
Q

What do F cells do?

A

release pancreatic peptide

acts like a satiety signal like neuropeptide Y

ENRE (21 decks)

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