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Test 4 MCM Leesy > B2.085b - Tissues And Metabolism > Flashcards

B2.085b - Tissues And Metabolism Flashcards

1
Q

When ATP falls there is a need to stimulate catabolic processes and to suppress anabolic processes. What is increased to allow this to happen

A

AMP increases which activates AMPK

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2
Q

What does adenylate kinase do

A

Catalyze 2 ADP —>AMP + ATP

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3
Q

Adenylate kinase does what with respect to energy

A

Allows you to get all the energy out of the ATP molecules

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4
Q

What is the perfect sensor for detecting the energy status of the cell

A

AMP

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5
Q

Why is AMP a good sensor of energy status of the cell

A

Its concentration is very low so when ATP breaks down and creates AMP it concentration change is very noticeable to enzymes

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6
Q

How is AMPK activated

A

CaMKK and LKB1 phosphorylation it

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7
Q

What does LKB1 respond to to cause it to phosphorylate AMPK

A

Increase in AMP:ATP ratio

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8
Q

What does CaMKK respond to to phosphorylate AMPK

A

Calcium

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9
Q

What does AMPK do

A

Increases energy production and inhibits energy expenditure

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10
Q

What type of effect does AMPK have on skeletal muscle

A

Insulin like

Increases transcription and translocation of GLUT 4

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11
Q

Chronic exercise increases what

A

Phosphorylation of PGC1alpha which stimulates biogenesis of mitochondria

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12
Q

AMPK has what effect in the liver

A

Inhibits acetyl CoA carboxylase

Decreases fatty acid synthesis and increases oxidation (relieves inhibition CPT1)

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13
Q

What does AMPK do in the liver with respect to cholesterol

A

Inhibits HMG-CoA reductase which inhibits cholesterol synthesis

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14
Q

What does AMPK do with respect to glucose

A

Inhibits glucose synthesis by inhibiting PEPCK

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15
Q

What does AMPK do with respect to hypothalamus

A

Increases appetite

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16
Q

What underlies cholesterol’s pathological effects

A

Its waxiness and ability to infiltrate membranes

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17
Q

What is cholesterol a precursor for

A

Bile salts
Steroid hormones
Vitamin D3

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18
Q

How are cholesterol esters stored

A

Fat droplets

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19
Q

Cholesterol modulates membranes what

A

Fluidity

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20
Q

The higher the cholesterol content in the membrane the

A

Less fluid the membrane

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21
Q

All 27 carbons of cholesterol are derived from what

A

Acetyl CoA

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22
Q

Where does cholesterol synthesis happen in the cell

A

Cytosol and ER

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23
Q

HMG CoA is a precursor for the synthesis of what other than cholesterol

A

Ketone bodies

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24
Q

What determines if HMG CoA is going to turn into Ketone bodies or cholesterol

A

If its in mitochondria it will go to ketone bodies if its in cytosol cholesterol

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25
Q

The production of mevaolonate by reduction fo HMG CoA is

A

The committed step and major site of control of cholesterol synthesis

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26
Q

What are ways HMG CoA is regulated

A

Transcription, phosphorylation and degradation

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27
Q

Where is HMG CoA reductase found

A

ER

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28
Q

What is the orientation of HMG CoA in the ER

A

Its a transmembrane helical domain that can bind to sterols and the C terminal catalytic domain that catalyze the reaction faces the cytosol

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29
Q

How do statins work

A

They are tight binding competitive inhibitors of the enzyme HGM CoA reductase

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30
Q

Describe the reaction of making cholesterol

A

HMG CoA —> Mevalonate –> squalene–> 27 C cholestrol

31
Q

What is the energy sourse of HMG CoA reductase

A

2 NADPH

32
Q

What classic paper from schoenheimer and breusch was published

A

First example of biological feedback system

33
Q

The classic paper from Gould et al. Showed what

A

First studies to use radioisotopes to measure the synthesis of cholesterol

34
Q

What controls cholesterol metabolism at the level of gene transcription

A

When cells are low in sterols SCAP transports SREBP2 from ER to Golgi. Release of SREBP from membrane is initiated by S1P, a protease that cleaves SREBPs in the luminal loop. SREBP that’s cleaved enters the nucleus where it activates the genes controlling lipid synthesis and uptake.

35
Q

SREBP is a transcription factor that up-regulates transcription of what

A

HMG CoA reductase and LDL receptor

36
Q

What prevents the movement of SCAP and SREBP complex from ER to Golgi?

A

Cholesterol in the membrane of ER

37
Q

What proteins are in the chylomicrons

A

ApoE, Apo CII, Apo B-48

38
Q

What do chylomicrons do

A

Transport dietary fats

Transports triglycerides to peripheral tissues and then to the liver

39
Q

What proteins are in VLDLs

A

Apo E, Apo CII, Apo B100

40
Q

What do VLDLs do

A

Made in liver and Apo B100 levels are linked to TG synthesis
Transports endogenous fats
Converted to IDL —> LDL by LPL and HDL

41
Q

What proteins are in LDL

A

Apo B 100

42
Q

What do LDLs do

A

Transport cholesterol from liver to peripheral tissues

Uptake receptor mediates endocytosis in liver and peripheral cells

43
Q

What are the proteins in HDL

A

Apo A, Apo E, Apo CII

44
Q

What does HDL do

A

Transports cholesterol from peripheral tissues to liver

45
Q

In the blood what helps hydrolyze the triglyceride from the chylomicrons

A

LPL

46
Q

Why are IDLs smaller but more dense

A

They have less triglycerides

47
Q

What protein picks up cholesterol from tissues

A

ApoA 1

48
Q

What is the process of LDLs getting taken up by a peripheral tissue

A
  1. Binds to LDL receptor
  2. Endosome/lysosome take it up
  3. Cholesterol gets released
49
Q

Cholesterol inhibits what and enhances what in the cell its taken up in

A

Inhibits
1. Acyl CoA
2. LDL receptor synthesis
Enhances
1. ABCA1 transporter - moves cholesterol out of the cell
2. ACAT - converts it to cholesterol ester (to make it a fat droplet) if there’s too much

50
Q

Normal half life of LDL

A

2 days

51
Q

How do statins decrease cholesterol

A

The inhibit HMG CoA Reductase

Upregulated LDL receptor in cells

52
Q

What does Type II Familial hypercholesterolemia do

A

Defective LDL receptor

Defective Apo B 100

53
Q

What happens to peripheral cells in people with T2 Familial hypercholesterolemia

A

HMG CoA reductase activated to provide sufficient cholesterol
LDLs stay in the blood bc there’s no LDL receptors

54
Q

When LDL receptors are defective what happens to the LDLs in the blood

A

Taken up by macrophages to make foam cells leading to plaques

55
Q

What metabolic defects can lead to development of hepatic steatosis

A

Increased lipolysis

Hyperglycemia/hyperinsulinemia

56
Q

What’s the most common way of getting a fatty liver

A

Obesity

57
Q

Insulin resistance

A

Decreased in target cell metabolic response to insulin

58
Q

What is insulin resistance due to

A

Nutritional excess and obesity but exact mechanism is unresolved

59
Q

What’s a major difference between TI and TI diabetes

A

In type to its insulin resistance but that doesn’t prevent insulin stimulation of lipid synthesis

60
Q

What is good fat

A

Subcutaneous

61
Q

What is bad fat

A

Visceral

62
Q

How is fat stored and why is it dangerous

A

As TGs but with a small/proportional DG. DG is bad because it activates PKCs that interferes with insulin and cause insulin resistance.

63
Q

In insulin resistance why do you still have fat storage stimulated by insulin but not an inhibition of glucose

A

They are separate insulin pathways that control them

64
Q

What is ethanol metabolized to

A

Acetaldehyde and acetate

65
Q

What does acetaldehyde converting to acetate do

A

Makes a lot of NADH which Inhibits gluconeogenesis and creates VLDLs

66
Q

The conversion of ethanol to acetaldehyde causes what

A

Drives a highly deuces cytoplasmic NAD+ redox state. Most of the NAD+ is in the NADH form.

67
Q

Low ratio of NAD+/NADH causes what

A

Reduces the rate of why gluconeogensis by reducing the concentration of pyruvate

68
Q

Low ratio of NAD+/NADH reduces gluconeogensis because

A

It reduces concentration of pyruvate, you need Lactate and NAD+ to make pyruvate so you increase Lactate concentration

69
Q

What is also inhibited by acetaldehyde

A

Fatty acid oxidation bc of low NAD+/NADH ratio. NAD+ is needed for ketone synthesis

70
Q

Ethanol decreases activity of

A

AMPK activity

PPAR alpha - decreased fatty acid oxidation

71
Q

What is increased by ethanol

A

SREBP-1 (TF) bc supply of too much fuel (ethanol)

so FFA synthesis is increased

72
Q

Ethanol causes what in ETC

A

Oxidative stress

73
Q

Alcohol abuse leads to ROS how

A

Acetaldehyde —>Schiff base—>AA-AGE —> NADPH oxidase —>ROS

Test 4 MCM Leesy (6 decks)

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