Cholestrol Synthesis Flashcards

(38 cards)

1
Q

What is found in excess in the liver in both fasted and fed state?

A

Acetyl CoA

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2
Q

What is the key enzyme in cholesterol synthesis?

A

HMG-CoA reductase

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3
Q

What stimulates HMG-CoA reductase?

A

Insulin

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4
Q

What inhibits HMG-CoA reductase?

A

AMPK (AMP-activated protein kinase)

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5
Q

What stimulates AMPK?

A

AMP stimulates it large amounts of ATP breakdown creates AMP

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6
Q

What inhibits AMPK?

A

Phosphocreatine

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7
Q

What does a deficiency in liver kinase B cause?

A

Doesn’t uptake glucose leaving it in the bloodstream hyperglycemia

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8
Q

What increases AMPK activity?

A

Leptin and adiponectin

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9
Q

What does AMPK cause?

A

Energy producing processes and decreases energy consuming processes

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10
Q

What breaks down HMG-CoA reductase?

A

Ubiquitin

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11
Q

What inhibits HMG-CoA and why?

A

Glucagon and epinephrine so you do not waste energy on cholesterol during fight or flight or fasted states

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12
Q

What does Insig do?

A

Holds SCAP-SREBP complex in ER in presence of sufficient cholesterol concentrations

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13
Q

What occurs to the SCAP-SREBP complex once cholesterol levels decrease?

A

Insig releases it and it SCAP-SREBP continues to the Golgi

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14
Q

What occurs to Insig once the SCAP-SREBP complex leaves the ER?

A

It is ubiquinated for proteolysis

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15
Q

Once in the Golgi what occurs to the SCAP-SREBP complex?

A

SREBP is cleaved from SCAP by MBTPS1

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16
Q

What occurs once SCAP is released from SREBP?

A

MBTPS2 cleaves it releasing the transcription factor

17
Q

What does ACAT do and why?

A

Esterifies cholesterol so that it can be transported and stays out of the membrane

18
Q

What occurs with a defect in ApoE?

A

IDL and chylomicrons remain in circulation too long causing hyperlipoproteinemia

19
Q

What does LCAT add to cholesterol?

A

Phosphatidylcholine instead of a fatty acid (ACAT fatty acid)

20
Q

Where does HDL get a fatty acid for esterification?

A

Its own membrane (no TAGs intracellularly)

21
Q

What receptor allows for LDL to be taken in by cells?

22
Q

What occurs to LDL once inside the cell?

A

Transported to lysosomes to breakdown everything and receptor sent up to surface again

23
Q

What is the transcription of HMG-CoA reductase dependent on?

A

Intracellular cholesterol concentration

24
Q

What is the rate limiting step of steroid synthesis?

25
What is StAR?
Protein responsible for transport of cholesterol into the mitochondria
26
What is the first step in synthesis of all steroid hormones?
Cholesterol to progestagens
27
What do progestagens get turned into?
Mineralocorticoids Glucocorticoids Androgens
28
What do estrogens come from?
Androgens
29
What enzyme is needed for androgens to turn to estrogens?
Aromatase
30
Where are progestagens made?
Adrenal cortex, gonads, CNS
31
Androgens are made:
Adrenal cortex and gonads
32
Mineralocorticoids/glucocorticoids are made:
Adrenal cortex
33
Estrogens are made:
Gonads
34
When and where are estriols made?
Only in pregnancy by fetal adrenal glands, liver and placenta
35
What is dihydrotestosterone?
5% of test is turned into this has a huge affect on secondary sex characteristics not primary characteristics
36
What enzyme converts testosterone to dihydrotestosterone?
5 alpha-reductase
37
What can 5 alpha-reductase deficiency lead to?
Male patterned baldness, benign prostatic hyperplasia, and prostate cancer
38
What can aromatase deficiency lead to?
In males and females no secondary sex characteristics