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

B2.085b - Tissues And Metabolism Flashcards

(73 cards)

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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
The production of mevaolonate by reduction fo HMG CoA is
The committed step and major site of control of cholesterol synthesis
26
What are ways HMG CoA is regulated
Transcription, phosphorylation and degradation
27
Where is HMG CoA reductase found
ER
28
What is the orientation of HMG CoA in the ER
Its a transmembrane helical domain that can bind to sterols and the C terminal catalytic domain that catalyze the reaction faces the cytosol
29
How do statins work
They are tight binding competitive inhibitors of the enzyme HGM CoA reductase
30
Describe the reaction of making cholesterol
HMG CoA —> Mevalonate --> squalene--> 27 C cholestrol
31
What is the energy sourse of HMG CoA reductase
2 NADPH
32
What classic paper from schoenheimer and breusch was published
First example of biological feedback system
33
The classic paper from Gould et al. Showed what
First studies to use radioisotopes to measure the synthesis of cholesterol
34
What controls cholesterol metabolism at the level of gene transcription
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
SREBP is a transcription factor that up-regulates transcription of what
HMG CoA reductase and LDL receptor
36
What prevents the movement of SCAP and SREBP complex from ER to Golgi?
Cholesterol in the membrane of ER
37
What proteins are in the chylomicrons
ApoE, Apo CII, Apo B-48
38
What do chylomicrons do
Transport dietary fats | Transports triglycerides to peripheral tissues and then to the liver
39
What proteins are in VLDLs
Apo E, Apo CII, Apo B100
40
What do VLDLs do
Made in liver and Apo B100 levels are linked to TG synthesis Transports endogenous fats Converted to IDL —> LDL by LPL and HDL
41
What proteins are in LDL
Apo B 100
42
What do LDLs do
Transport cholesterol from liver to peripheral tissues | Uptake receptor mediates endocytosis in liver and peripheral cells
43
What are the proteins in HDL
Apo A, Apo E, Apo CII
44
What does HDL do
Transports cholesterol from peripheral tissues to liver
45
In the blood what helps hydrolyze the triglyceride from the chylomicrons
LPL
46
Why are IDLs smaller but more dense
They have less triglycerides
47
What protein picks up cholesterol from tissues
ApoA 1
48
What is the process of LDLs getting taken up by a peripheral tissue
1. Binds to LDL receptor 2. Endosome/lysosome take it up 3. Cholesterol gets released
49
Cholesterol inhibits what and enhances what in the cell its taken up in
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
Normal half life of LDL
2 days
51
How do statins decrease cholesterol
The inhibit HMG CoA Reductase | Upregulated LDL receptor in cells
52
What does Type II Familial hypercholesterolemia do
Defective LDL receptor | Defective Apo B 100
53
What happens to peripheral cells in people with T2 Familial hypercholesterolemia
HMG CoA reductase activated to provide sufficient cholesterol LDLs stay in the blood bc there’s no LDL receptors
54
When LDL receptors are defective what happens to the LDLs in the blood
Taken up by macrophages to make foam cells leading to plaques
55
What metabolic defects can lead to development of hepatic steatosis
Increased lipolysis | Hyperglycemia/hyperinsulinemia
56
What’s the most common way of getting a fatty liver
Obesity
57
Insulin resistance
Decreased in target cell metabolic response to insulin
58
What is insulin resistance due to
Nutritional excess and obesity but exact mechanism is unresolved
59
What’s a major difference between TI and TI diabetes
In type to its insulin resistance but that doesn’t prevent insulin stimulation of lipid synthesis
60
What is good fat
Subcutaneous
61
What is bad fat
Visceral
62
How is fat stored and why is it dangerous
As TGs but with a small/proportional DG. DG is bad because it activates PKCs that interferes with insulin and cause insulin resistance.
63
In insulin resistance why do you still have fat storage stimulated by insulin but not an inhibition of glucose
They are separate insulin pathways that control them
64
What is ethanol metabolized to
Acetaldehyde and acetate
65
What does acetaldehyde converting to acetate do
Makes a lot of NADH which Inhibits gluconeogenesis and creates VLDLs
66
The conversion of ethanol to acetaldehyde causes what
Drives a highly deuces cytoplasmic NAD+ redox state. Most of the NAD+ is in the NADH form.
67
Low ratio of NAD+/NADH causes what
Reduces the rate of why gluconeogensis by reducing the concentration of pyruvate
68
Low ratio of NAD+/NADH reduces gluconeogensis because
It reduces concentration of pyruvate, you need Lactate and NAD+ to make pyruvate so you increase Lactate concentration
69
What is also inhibited by acetaldehyde
Fatty acid oxidation bc of low NAD+/NADH ratio. NAD+ is needed for ketone synthesis
70
Ethanol decreases activity of
AMPK activity | PPAR alpha - decreased fatty acid oxidation
71
What is increased by ethanol
SREBP-1 (TF) bc supply of too much fuel (ethanol) | so FFA synthesis is increased
72
Ethanol causes what in ETC
Oxidative stress
73
Alcohol abuse leads to ROS how
Acetaldehyde —>Schiff base—>AA-AGE —> NADPH oxidase —>ROS

Test 4 MCM Leesy (6 decks)

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