Lecture 17 - Fatty Acid Oxidation and Ketone Metabolism Flashcards Preview

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Flashcards in Lecture 17 - Fatty Acid Oxidation and Ketone Metabolism Deck (25)
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1

Conditions promoting FA catabolism from adipose tissue include fasting, physical exertion, and stress. What two major hormones are increased by physical exercise and stress?

1. Epinephrine
2. ACTH

2

Which is NOT a tissue that uses FA as a major fuel?

A. Liver
B. Muscle
C. Heart
D. RBCs
E. Kidney

D - RBCs can't oxidize FA because they don't have mitochondria.

3

_______ in the plasma binds free 99% of FFA.

Albumin

4

__________ binds FA that diffuse across membranes of tissues and, once bound, prevents them from diffusing out of the cell.

Fatty acid binding protein (FABP)

5

The regulated step in fatty acid oxidation involves what enzyme?

A. CAT-I
B. VLCAD
C. MCAD

A - inhibiting CAT-I essentially inhibits most FA oxidation since CAT-I is used to move long-chain FAs across the IMM.

6

How much ATP is generated from the total oxidation of palmitic acid to CO2 and H2O?

131 - 2 = 129 ATP

7

_________ deficiency leads to a decrease in the ability to oxidize FA; characterized by nonketonic hypoglycemia.

A. CAT-I
B. VLCAD
C. MCAD
D. Carnitine

A

8

_______ deficiency is the most common genetic defect in FA oxidation.

A. CAT-I
B. VLCAD
C. MCAD
D. Carnitine

C

9

_______ deficiency would lead to the most severe consequences because without it no long-chain FA can be oxidized.

A. CAT-I
B. VLCAD
C. MCAD
D. Carnitine

B

10

________ can form acyl-carnitines that are excreted, resulting in less carnitine available for the carnitine shuttle.

Low MW organic acids (such as valproic acid)

11

Peroxisomes are important for the oxidation of which two types of fatty acids?

1. Very long chain (VLCFA; C26+)
2. Branched chain

12

Where is Beta-oxidation in peroxisomes moved once the FAs are 8-10 carbons?

Mitochondria

13

Degradation of branched-chain amino acids is initiated by an __________.

a-oxidation pathway

14

________ is a genetic deficiency in alpha-hydroxylase, which initiates BCFA a-oxidation.

A. Zellweger Syndrome
B. Refsum's disease
C. Gaucher's disease
D. Tay Sach's disease

B

15

_________ is the absence of peroxisomes and the inability to synthesize plasmalogens.

A. Zellweger Syndrome
B. Refsum's disease
C. Gaucher's disease
D. Tay Sach's disease

A - there is no treatment for Zellweger Syndrome.

16

Acetyl-CoA carboxylase (ACC) is ALLOSTERICALLY activated by:

A. Citrate
B. Glucagon
C. Insulin
D. Malonyl-CoA

A

17

ACC produces _______ which inhibits CAT-I.

A. Citrate
B. Glucagon
C. Insulin
D. Malonyl-CoA

D

18

_______ is activated by glucagon via cAMP-dependent phosphorylation.

A. CAT-I
B. Acetyl-CoA carboxylase (ACC)
C. Hormone-Sensitive Lipase

C

19

_______ is hormonally activated by insulin via dephosphorylation.

A. CAT-I
B. Acetyl-CoA carboxylase (ACC)
C. Hormone-Sensitive Lipase

B

20

What are the two major types of ketone bodies?

1. Acetoacetate
2. B-hydroxybutyrate

21

_________ is the enzyme that condenses 2 acetyl-CoA to get acetoacetyl-CoA (a reversible reaction).

A. HMG-CoA synthase
B. HMG-CoA lyase
C. Thiolase
D. B-hydroxybutyrate DH

C

22

______ adds another acetyl-CoA to acetoacetyl-CoA to get hydroxymethylglutaryl-CoA.

A. HMG-CoA synthase
B. HMG-CoA lyase
C. Thiolase
D. B-hydroxybutyrate DH

A

23

___________ catalyzes cleavage into acetoacetate and acetyl-CoA.

A. HMG-CoA synthase
B. HMG-CoA lyase
C. Thiolase
D. B-hydroxybutyrate DH

B

24

________ uses NADh to convert acetoacetate to B-hydroxybutyrate (a reversible reaction).

A. HMG-CoA synthase
B. HMG-CoA lyase
C. Thiolase
D. B-hydroxybutyrate DH

D

25

_________ is the most prevalent lysosomal storage disorder.

A. Zellweger Syndrome
B. Refsum's disease
C. Gaucher's disease
D. Tay Sach's disease

C