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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
why lipids efficient energy source (other than more ATP)
1g TGs stored in 1g adipose tissue (Hoffer: a bit more) | 1g glycogen stored in 2-3g of hepatocytes bc has water moieties
26
liver role in maintaining blood glucose and how
GNG from pyruvate, lactate and OAA. export glucose out to keep glycemia
27
problem of severe nutritional insufficiency for the TCA cycle
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
3 ketone bodies
acetone, acetoacetate, beta-hydroxybutyrate
29
1st step of ketone body synthesis
2 acetyl-CoA make acetoacetyl-CoA (+ free CoA)
30
2nd step of ketone body synthesis
acetoacetyl-CoA combined with acetyl-CoA by HMG-CoA synthase (rate limiting enzyme of cholesterol synthesis pathway) to make HMG-CoA (6C)
31
HMG-CoA (6C) 2 things that can happen to it
1. cholesterol synthesis pathway | 2. nutritional deficiency: other pathway to form ketone bodies
32
3rd step of ketone bodies synthesis (what happens to HMG-CoA)
acetyl-CoA removed from it, yielding acetoacetate (4C)
33
2 things that can happen to acetoacetate (4C)
1. spontaneously becomes acetone in the blood | 2. becomes 3-hydroxybutarate (by 3-hydroxybutarate dehydrogenase)
34
ketone bodies: what cells use them and benefits of adaptation to using them as fuel
brain and muscle (adapt to use them in long term fasting, spares some prot breakdown and GNG)
35
condition where ketone bodies made
type 1 diabetes.
36
insulin deficiency: why take ketone bodies (in fat and muscle)
no insulin signaling to insert glut4 in fat and muscle cells
37
insulin deficiency effect on liver
no inhibition of glycogenolysis and GNG. more glucose added to the blood, making hyperglycemia even worse
38
fat metabolism in the absence of insulin
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
why get ketoacidosis in type 1 DM but not type 2 DM or fasting
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
how insulin acts to inhibit lipolysis in adipose tissue: 1st step
binds RTK and phosphorylation cascade starts
41
how insulin acts to inhibit lipolysis in adipose tissue: 2nd step (after RTK phosph cascade)
a phosphatase is activated and removes phosph from HSL (opposite of PKA effect)
42
how DKA can occur in type 2 DM
DM 2 for long time + resistance + secretion defect got worse + other stress (infection, heart attack, etc.)
43
other reason insulin deficiency promotes ketosis (other than lipolysis occuring)
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
consequence of FA going in mt due to insulin deficiency leading to malonyl-CoA prod
FA made into acetyl-CoA and acetyl-CoA becomes ketone bodies
45
normal ketosis states (mild) and why
- 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
pathophgy ketosis
- DM type 1 - ingestion of ethanol or salicylates (severe overdose) - inborn errors of metabolism
47
compensatory mechanism for DKA
tachypnea (often Kussmaul breathing: rapid deep breathing)
48
consequences of hyperglycemia on kidneys
osmotic diuresis, drags Na with it, loss of volume, hypotn
49
acidosis (of ketone bodies) consequence on potassium
hyperK bc H+ K+ antiporters in alpha intercalated cells in CT work harder
50
acronym and meaning for diabetes treatment
D: treat Diabetes E: electrolytes A: acidosis D: dehydration
51
DEAD acronym first D meaning
give insulin to treat Diabetes
52
DEAD acronym E meaning
treat hyperK, helped with insulin, and start to give K when normoK otherwise get hypoK bc of insulin
53
DEAD acronym A meaning
treat acidosis (may give bicarb if pH below 7)
54
DEAD acronym 2nd D meaning
dehydration (infuse isotonic saline)
55
best diabetes treatment to avoid hypoglycemia
GLP-1 bc only stimulates insulin when blood glucose is high
56
threshold before get neuroglycopenic symptoms and why
glucose of 2 mM or less bc then impaired glucose transport to brain via glut 1 (which has Km of 1)
57
how brain protects itself from the glucose of 2 mM or less
activates counterregulatory hormone response (through peripheral SS nerves)
58
couterregulatory hormone response def
SS nerves to periphery: 1. turn on glucagon secretion (alpha cells) 2. NE and E from adrenals 3. cortisol via ACTH pathway
59
effect of glucagon, NE, E and cortisol to protect from hypoglycemia
1. activate glycogenolysis 2. activate lipolysis for GNG 3. cortisol activates GNG enzymes and protein breakdown
60
why counterregulatory hormone response may not work in prolonged diabetes
get nerve damage so SS nerves don't work. get fuzzy in their head and neuro symptoms
61
high insulin: how much glucose is released from the liver and consequence if forget to take a meal with insulin
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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