Lecture 15 - Cholesterol Metabolism Flashcards

1
Q

__________ is the source of all carbons in synthesized cholesterol.

A

Acetyl-CoA

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2
Q

___________ is 6 carbons and formed from 3 acetyl-CoA.

A

HMG-CoA

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3
Q

What is the major regulated enzyme in the cholesterol biosynthetic pathway?

A

HMG-CoA reductase

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4
Q

The activity of HMG-CoA reductase is increased by:

A. Thyroid hormone
B. Glucagon
C. Cortisol
D. All of these
E. None of these
A

A

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5
Q

The activity of HMG-CoA reductase is decreased by:

A. Thyroid hormone
B. Insulin
C. Cortisol
D. All of these
E. None of these
A

C

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6
Q

The synthesis of HMG-CoA reductase is repressed by:

A. Thyroid hormone
B. Glucagon
C. Cortisol
D. Cytosolic cholesterol
E. Insulin
A

D

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7
Q

Which is NOT a product of the reaction that is catalyzed by HMG-CoA reductase?

A. Mevalonate
B. CoASH
C. HMG-CoA
D. NADP+

A

C - this is a reactant, which is combined with NADPH to yield mevalonate, CoASH, and 2 NADP+.

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8
Q

Absorption and uptake of DIETARY cholesterol reaches the liver via what primary mechanism?

A. Chylomicron remnants
B. Extra hepatic de novo synthesis of cholesterol
C. Secretion of HDL from the liver
D. None of these
E. All of these
A

A

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9
Q

Extrahepatic de novo synthesis of cholesterol reaches the liver via ____.

A. IDL
B. Chylomicron remnants
C. HDL
D. LDL receptors

A

C

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10
Q

LDL binds to LDL-receptors on all cells via via what apoprotein?

A

Apo B-100

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11
Q

A deficiency in apoliprotein B results in hypercholesterolemia. This means there is more cholesterol in the ________ because it can not get into tissues.

A

plasma

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12
Q

What are 4 treatment options for hypercholesterolemia?

A

A. Statins
B. Cholestyramine
C. LIver transplant
D. LDL apheresis

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13
Q

__________ is involved with intracellular storage of cholesterol as cholesterol esters.

A. ACAT
B. LCAT
C. MCAT

A

A

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14
Q

__________ is involved with reverse transport of cholesterol, and associated with HDL.

A. ACAT
B. LCAT
C. MCAT
D. RCAT
E. HCAT
A

B

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15
Q

________ converts cholesterol to bile acids, which are the main excretory form of cholesterol.

A

The liver

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16
Q

How do statins work to treat hypercholesterolemia? (E.g. what do they inhibit?)

A

Statins inhibit HMG-CoA reductase,

a) limiting the synthesis of cholesterol from acetyl-CoA and
b) reducing back-up in the blood caused by lack of LDL receptors

17
Q

The carboxyl group on the side chain of the bile acids can form amide bonds with what two amino acids to form bile salts?

A
  1. glycine

2. taurine

18
Q

Cholic acid and chenodeoxycholic acid are examples of:

A

major bile acids

19
Q

What are two features of bile acids and bile salts that allow them to be good emulsifiers?

A
  1. Amphipathic (negative head group/neutral body)

2. Low pKa on side chain conjugated group

20
Q

___________ is the process of liver secretion and gut (small intestine reabsorption to the point where only about 5% of bile acids are excreted in the feces.

A

Enterohepatic circulation

21
Q

Bile acids are released into the lumen of the upper small intestine and then are reabsorbed by the lower small intestine into the portal circulation where they noncovalently bind __________.

A

albumin

22
Q

Which is activated by free cytosolic cholesterol?

A. HMG-CoA reductase
B. Synthesis of LDL receptors
C. ACAT
D. Synthesis and uptake of cholesterol

A

C - Free cytosolic cholesterol represses synthesis of HMG-CoA reductase and synthesis of LDL receptors, but ACTIVATES ACAT (meaning synthesis and uptake of cholesterol are reduced).