Insulin and metabolic reglation\ Flashcards

1
Q

3 pancreas endocrine cells and what they produce

A
  1. B cell - insulin, amylin, c-peptide
  2. a cell - glucagon
  3. omega cell - somatostatin
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2
Q

what triggers insulin release

A

glucose levels

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3
Q

what is the path by which glucose releases insuling in B cell

A
  1. glucose in > glycolysis and ATP production
  2. ATP inhibits K channel (less K out) reducing membrane potential
  3. membrane depolarization leads to Ca influx
  4. exocytosis of insulin post-Ca influx
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4
Q

how is insulin synthesized in B-cell

A
  1. DNA>mRNA>preproinsulin
  2. prepro has signal sequence removed and 3 disulfides formed > proinsulin
  3. proinsuling has c-peptide released and left with insulin
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5
Q

what is timing of insulin after meal (2)

A
  1. intial spike of exocytosis

2. slow gain as more is created after

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6
Q

6 stimulators of insulin

A
  1. glucose (major)
  2. AAs
  3. FFAs
  4. GLP-1
  5. glucagon
  6. Ach
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7
Q

3 inhibitors of insulin

A
  1. somatostatin
  2. insulin
  3. norepinepherine
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8
Q

how does microRNA inhibit insulin

A

binds to and inhibits translation of myotrophin mRNA, which is needed for secretion of vesicle

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9
Q

what are insulin’s role in anabolic processes (5)

A
  1. recruitment of glucose trnasporters for uptake
  2. stim glycogen synsthesis and inhib glycogen breakdown
  3. increase FA synthesis
  4. upregulate glucokinase
  5. increase AA uptake and protein synthesis
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10
Q

how does insuling promote gulcose uptake

A

insulin binding triggers vesicle carryin GLUT4 transporter to go to cell membrane surface

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11
Q

aside from insulin, what else can recruit transporters

A

exercise

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12
Q

how does insulin signalling work?

A
  1. insulin binds to receptor
  2. tyrosine kinase activated protein kinases
  3. protetin kinase phosphoryalte other proteins, causing them to signal
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13
Q

how does insulin reverse effects of glucagon and epi

A
  1. both glucagon and epi phosphorylate glycogen phosphorylase a, which leads to glycogen breakdown
  2. insulin activates protein phophotase, which dephosphorylates thise enzyme, inhibiting glycogen breakdown
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14
Q

how does glucose enter the liver

A

down concentration gradient

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15
Q

how are low intracellular glucose level maintained (3)

A
  1. glucose phosphoryalted
  2. glycogen synthesis
  3. reduced glycogen breakdown
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16
Q

3 proteins involved

A
  1. GLUT2
  2. glucokinase
  3. glycogen synthase
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17
Q

what is glucagon released

A

what gluc. drops below 100mg/dL

18
Q

how does glucagon prevent hypoglycemia

A

increases liver glycogenolysis and gluconeogenisis

19
Q

what is glucagon signalling pathway

A

GCPRs and phosphorylation cascade

20
Q

2 other results of glucagon

A
  1. beta oxidatiokn

2. ketogenisis

21
Q

3 possible products of proglucagon and where from/functions

A
  1. glucagon - a cells of panc
  2. GLP-1 - endocrine of small int. - insulin release
  3. GLP-2 - intestine endocrine - inhibit food intake
22
Q

what do somatostatins do

A

inhibit endo and exocrine secretions

23
Q

how is amylin secreted

A

from islet with insulin

24
Q

location and Function of amylin action (3)

A
  1. stomach - slows emptying and slows acid secretion
  2. brain - decreases appetite
  3. pancreas - decrease glucagon secretions
25
Q

what is type 1 diabetes

A

autoimmune destruction of B cells

26
Q

what must be regulated in type 1 (3)

A
  1. insulin
  2. carb intake
  3. physical activity
27
Q

7 risk factors for diabetic hypoglycemia

A
  1. bad insulin dosing
  2. skipped meals of snacks
  3. reduced dietary carbs
  4. increased glucose usage (excercise)
  5. decreased gluconeogenisis (alcohol)
  6. increased insulin sensititvety
  7. decreased insulin clearance (renal)
28
Q

how to treat hypoglycemia

A

glucose

29
Q

4 Sx of hyperglycemia

A
  1. fluid intake and thisrt
  2. frequent urination
  3. high ketones (sweet breath)
  4. glucosuria
  5. rapid deep breath (acidosis)
  6. high blood tonicity (results in K loss)
30
Q

how does hyperglycemia cause retinal damage

A

glucose converted to sorbitol

31
Q

how does hyperglycemia cause ketosis

A

excess fat breakdown leads to ketones

32
Q

what happens when not enough glucose in cell

A

break down fat and protein instead

33
Q

where does ketogenisis occur

A

in mitochondira when acetyl CoA levels rise

34
Q

what are the 3 ketone bodies produced

A
  1. acetoacetate
  2. 3-hydroxybutyrate
  3. acetone
35
Q

what are ketone used for

A

alternative E source by bain, heart and muscle

36
Q

how does body use ketone bodies as fuel

A

1 3-hydroxybutyrate converted to 2 actyl CoA

37
Q

why does citric acid cycle slow without glucose

A

pyruvate not replensihed

38
Q

what are consequences of high ketones

A

drop in blood pH - ketoacidosis

39
Q

how is ketoacidosis treated

A

life threatening - bicarb injections

40
Q

what is path of ketogenisis

A
  1. no glucose so FFA are release from adipose
  2. FFAs undergo B-oxidation in liver
  3. ketone bodies formed
41
Q

how does diabetes effect water balance

A
  1. high glucose and ketone > hypertonicity
  2. dehydration due to hypertonicity
  3. polyuria to get rid of water in blood
  4. water loss leads to hypotension
  5. low BP can lead to loss of consciousness
  6. kidney failure due to excessive processing