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GI Exam 2 > Cholestrol Synthesis > Flashcards

Cholestrol Synthesis Flashcards

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?

A

Apo B

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?

A

StAR

25
Q

What is StAR?

A

Protein responsible for transport of cholesterol into the mitochondria

26
Q

What is the first step in synthesis of all steroid hormones?

A

Cholesterol to progestagens

27
Q

What do progestagens get turned into?

A

Mineralocorticoids
Glucocorticoids
Androgens

28
Q

What do estrogens come from?

A

Androgens

29
Q

What enzyme is needed for androgens to turn to estrogens?

A

Aromatase

30
Q

Where are progestagens made?

A

Adrenal cortex, gonads, CNS

31
Q

Androgens are made:

A

Adrenal cortex and gonads

32
Q

Mineralocorticoids/glucocorticoids are made:

A

Adrenal cortex

33
Q

Estrogens are made:

A

Gonads

34
Q

When and where are estriols made?

A

Only in pregnancy by fetal adrenal glands, liver and placenta

35
Q

What is dihydrotestosterone?

A

5% of test is turned into this has a huge affect on secondary sex characteristics not primary characteristics

36
Q

What enzyme converts testosterone to dihydrotestosterone?

A

5 alpha-reductase

37
Q

What can 5 alpha-reductase deficiency lead to?

A

Male patterned baldness, benign prostatic hyperplasia, and prostate cancer

38
Q

What can aromatase deficiency lead to?

A

In males and females no secondary sex characteristics

GI Exam 2 (20 decks)

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