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Bloc E - GI & Metabolism > Feb9 M2-Lipid Metabolism 2 > Flashcards

Feb9 M2-Lipid Metabolism 2 Flashcards

1
Q

first step for lipid breakdown (adipose tissue) and mobilization

A

signal tells to do so (catabolic hormones like glucagon and E) binds to a GPCR with Gs protein

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2
Q

2nd step for lipid breakdown (adipose tissue) and mobilization (after Gs activated)

A

Gs couples to adenylyl cyclase. converts ATP to cAMP to turn on other enzymes like PKA

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3
Q

3rd step for lipid breakdown (adipose tissue) and mobilization (2 things active PKA does)

A
  1. PKA phosph a protein called hormone sensitive lipase (sensitive to glucagon and E)
  2. PKA phosph protein coating lipid droplets called perilipin
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4
Q

4th step for lipid breakdown (adipose tissue) and mobilization (effect of phosph perilipin and HSL, hormone sensitive lipase)

A

phosph of perilipin allows access to TGs to the HSL and it hydrolyzes TGs to FAs

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5
Q

5th step of lipid breakdown (adipose tissue) and mobilization (what happens to FAs obtained from HSL breaking TGs)

A

exported into the blood bound to albumin. have diff fates but ultimately oxidized for energy

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6
Q

what hormone can inhibit lipid breakdown (adipose tissue) and mobilization

A

insulin

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7
Q

key cell type taking FAs and oxidizing them for energy and how

A

SKM. through FA transporter

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8
Q

getting FAs in mt 1st step

A

FA is bound to CoA and moves to IMS (crosses OMM)

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9
Q

getting FAs n mt 2nd step

A

carnitine palmitoyl transferase 1 (CPT1), a OMM enzyme, fuses FA-CoA with carnitine to make it carnito-palmitoyl molecule and the CoA is released

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10
Q

getting FAs in mt 3rd step

A

carnito-palmitoyl recognized by a translocase on IMM (FA needed carnitine for this to happen) and moves it to matrix

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11
Q

getting FAs in mt 4th step

A

CPT2, a IMM enzyme, makes carnino-palmitoyl molecule into FA-CoA and carnitine is released

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12
Q

getting FAs in mt: how carnitine gets back to IMS to get recycled and doesn’t accum in matrix

A

translocase moves it from matrix (after CPT2 rx) to IMS so can be used agian in CPT1 rx

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13
Q

CPT1 regulation and in what cells

A

malonyl-CoA, product of ACC (acetyl-CoA carboxylase) in FA synthesis, inhibits CPT1 in the liver so CPT1 highly regulated rate-limiting step (very sensitive to malonyl-CoA)

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14
Q

consequence of defect in pathway getting FA in mt

A

ATP deficiency and leads to hypoglycemia bc need ATP to make glucose

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15
Q

carnitine deficiency causes

A
  • severe liver disease (problem in carnitine synthase in the liver, that makes carnitine in the liver
  • severe malnutrition or strict vegan diet
  • CPT1 or CPT2 mutation
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16
Q

beta-oxidation of FAs in mt is what basically

A

sequence of rxs similar to FA synthesis but in reverse and done by another reverse set of enzymes

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17
Q

1st step of beta oxidation

A

dehydration (dehydrate double carbon to make a double bond: acyl-CoA dehydrogenase. makes FADH2 from FAD !)

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18
Q

2nd step of beta oxidation (what happens to 2-transenoyl-CoA

A

hydration
2-transenoyl-CoA (FA-CoA with double bond at carb2) has hydroxyl group on C3 and double bond is gone: yield 3-hydroxyacyl-CoA

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19
Q

3rd step of beta oxidation (what happens to 3-hydroxyacyl-CoA)

A

ketone group (dehydration) made from hydroxyl on C3 that is dehydrated. makes 3-ketoacyl-CoA. made NADH from NAD

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20
Q

4th step of beta oxidation (what happens to 3-ketoacyl-CoA)

A

cleave off first 2 carbons and leave a new acyl-CoA molecule shorter of 2 carbons and bound to CoA.

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21
Q

enzyme making 4th step of beta oxidation (cleaving 2 Cs from 3-ketoacyl-CoA) and name of product made

A

thiolase (beta-ketoacyl-CoA thiolase). makes acyl-CoA (like in beginning but 2C less

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22
Q

summary of beta oxidation steps (4) + useful products obtained just with that (not considering acetyl-CoA will go in TCA cycle)

A
  • dehydration (make double bond on C2)
  • hydration (C3)
  • dehydration to make ketone group (C3)
  • cleave first 2C
  • got 1 NADH + 1 FADH2 for each 2C
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23
Q

common enzyme deficiency in beta oxidation

A

acyl-CoA dehydrogenase deficiency (first enzyme making the double bond)

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24
Q

how many ATP molecules do acetyl-CoA, NADH,FADH, palmitate and glucose each make

A 
acetyl-CoA = 12
NADH = 3
FADH = 2
palmitate = 131 (129 if removed 2 ATPs needed to make acyl-CoA
glucose = 36
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25
Q

why lipids efficient energy source (other than more ATP)

A

1g TGs stored in 1g adipose tissue (Hoffer: a bit more)

1g glycogen stored in 2-3g of hepatocytes bc has water moieties

26
Q

liver role in maintaining blood glucose and how

A

GNG from pyruvate, lactate and OAA. export glucose out to keep glycemia

27
Q

problem of severe nutritional insufficiency for the TCA cycle

A

cycle metabolites used in GNG so can’t oxidize acetyl-CoA in TCA cycle anymore (no more OAA, etc.) so aceytl-CoA goes in diff pathways to make ketone bodies

28
Q

3 ketone bodies

A

acetone, acetoacetate, beta-hydroxybutyrate

29
Q

1st step of ketone body synthesis

A

2 acetyl-CoA make acetoacetyl-CoA (+ free CoA)

30
Q

2nd step of ketone body synthesis

A

acetoacetyl-CoA combined with acetyl-CoA by HMG-CoA synthase (rate limiting enzyme of cholesterol synthesis pathway) to make HMG-CoA (6C)

31
Q

HMG-CoA (6C) 2 things that can happen to it

A
  1. cholesterol synthesis pathway

2. nutritional deficiency: other pathway to form ketone bodies

32
Q

3rd step of ketone bodies synthesis (what happens to HMG-CoA)

A

acetyl-CoA removed from it, yielding acetoacetate (4C)

33
Q

2 things that can happen to acetoacetate (4C)

A
  1. spontaneously becomes acetone in the blood

2. becomes 3-hydroxybutarate (by 3-hydroxybutarate dehydrogenase)

34
Q

ketone bodies: what cells use them and benefits of adaptation to using them as fuel

A

brain and muscle (adapt to use them in long term fasting, spares some prot breakdown and GNG)

35
Q

condition where ketone bodies made

A

type 1 diabetes.

36
Q

insulin deficiency: why take ketone bodies (in fat and muscle)

A

no insulin signaling to insert glut4 in fat and muscle cells

37
Q

insulin deficiency effect on liver

A

no inhibition of glycogenolysis and GNG. more glucose added to the blood, making hyperglycemia even worse

38
Q

fat metabolism in the absence of insulin

A

don’t store lipid bc no inhibition of TGs mobilization and breakdown in adipose tissue. FAs go to liver and mostly make ketone bodies

39
Q

why get ketoacidosis in type 1 DM but not type 2 DM or fasting

A

type 2 DM and fasting: still have the basal insulin so can inhibit lipolysis in adipose tissue (no basal insulin in type 1 DM)

40
Q

how insulin acts to inhibit lipolysis in adipose tissue: 1st step

A

binds RTK and phosphorylation cascade starts

41
Q

how insulin acts to inhibit lipolysis in adipose tissue: 2nd step (after RTK phosph cascade)

A

a phosphatase is activated and removes phosph from HSL (opposite of PKA effect)

42
Q

how DKA can occur in type 2 DM

A

DM 2 for long time + resistance + secretion defect got worse + other stress (infection, heart attack, etc.)

43
Q

other reason insulin deficiency promotes ketosis (other than lipolysis occuring)

A

remember insulin activates a protein phosphatase that removes P from ACC (acetyl-CoA carboxylase to activate it and malonyl-CoA made (inhibitor of FA uptake in mt). So FA uptake in mt happens now.

44
Q

consequence of FA going in mt due to insulin deficiency leading to malonyl-CoA prod

A

FA made into acetyl-CoA and acetyl-CoA becomes ketone bodies

45
Q

normal ketosis states (mild) and why

A
  • newborn (fasting before gets milk)
  • pregnancy: insulin resistance (less efficient to block lipase + increased needs of fetus in 3rd semester)
  • prolonged exercise
  • high fat diet
46
Q

pathophgy ketosis

A
  • DM type 1
  • ingestion of ethanol or salicylates (severe overdose)
  • inborn errors of metabolism
47
Q

compensatory mechanism for DKA

A

tachypnea (often Kussmaul breathing: rapid deep breathing)

48
Q

consequences of hyperglycemia on kidneys

A

osmotic diuresis, drags Na with it, loss of volume, hypotn

49
Q

acidosis (of ketone bodies) consequence on potassium

A

hyperK bc H+ K+ antiporters in alpha intercalated cells in CT work harder

50
Q

acronym and meaning for diabetes treatment

A

D: treat Diabetes
E: electrolytes
A: acidosis
D: dehydration

51
Q

DEAD acronym first D meaning

A

give insulin to treat Diabetes

52
Q

DEAD acronym E meaning

A

treat hyperK, helped with insulin, and start to give K when normoK otherwise get hypoK bc of insulin

53
Q

DEAD acronym A meaning

A

treat acidosis (may give bicarb if pH below 7)

54
Q

DEAD acronym 2nd D meaning

A

dehydration (infuse isotonic saline)

55
Q

best diabetes treatment to avoid hypoglycemia

A

GLP-1 bc only stimulates insulin when blood glucose is high

56
Q

threshold before get neuroglycopenic symptoms and why

A

glucose of 2 mM or less bc then impaired glucose transport to brain via glut 1 (which has Km of 1)

57
Q

how brain protects itself from the glucose of 2 mM or less

A

activates counterregulatory hormone response (through peripheral SS nerves)

58
Q

couterregulatory hormone response def

A

SS nerves to periphery:

  1. turn on glucagon secretion (alpha cells)
  2. NE and E from adrenals
  3. cortisol via ACTH pathway
59
Q

effect of glucagon, NE, E and cortisol to protect from hypoglycemia

A
  1. activate glycogenolysis
  2. activate lipolysis for GNG
  3. cortisol activates GNG enzymes and protein breakdown
60
Q

why counterregulatory hormone response may not work in prolonged diabetes

A

get nerve damage so SS nerves don’t work. get fuzzy in their head and neuro symptoms

61
Q

high insulin: how much glucose is released from the liver and consequence if forget to take a meal with insulin

A

none bc promotes storage of glucose to glycogen or breakdown to pyruvate. will have to mount couterregulatory hormone response

Bloc E - GI & Metabolism (58 decks)

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