1- Fatty acids are activated to acyl-coas and the acyl group is further transferred to carnitine because:

Section 10

Multiple Choice

1- Fatty acids are activated to acyl-CoAs and the acyl group is further transferred to carnitine because:

A) acyl-carnitines readily cross the mitochondrial inner membrane, but acyl-CoAs do not.

B) acyl-CoAs easily cross the mitochondrial membrane, but the fatty acids themselves will not.

C) carnitine is required to oxidize NAD+ to NADH.

D) fatty acids cannot be oxidized by FAD unless they are in the acyl-carnitine form. E) None of the above is true.

2- Which of the following is (are) true of the oxidation of 1 mol of palmitate (a 16-carbon saturated fatty acid; 16:0) by the β-oxidation pathway, beginning with the free fatty acid in the cytoplasm?

1. Activation of the free fatty acid requires the equivalent of two ATPs. 2. Inorganic pyrophosphate (PPi) is produced.

3. Carnitine functions as an electron acceptor. 4. 8 mol of FADH₂ are formed.

5. 8 mol of acetyl-CoA are formed.

6. There is no direct involvement of NAD+.

A) 1 and 5 only B) 1, 2, and 5 C) 1, 2, and 6 D) 1, 3, and 5 E) 5 only

3- Which of the following statements concerning the β oxidation of fatty acids is true? A) About 1,200 ATP molecules are ultimately produced per 20-carbon fatty acid oxidized. B) One FADH2 and two NADH are produced for each acetyl-CoA.

C) The free fatty acid must be carboxylated in the β position by a biotin-dependent reaction before the process of β oxidation commences.

D) The free fatty acid must be converted to a thioester before the process of β oxidation commences.

4- The following fatty acid, in which the indicated carbon is labeled with 14C, is fed to an animal:

14

CH₃(CH₂)₉COOH

After allowing 30 minutes for fatty acid β oxidation, the label would most likely be recovered in:

A) acetyl-CoA.

B) beta-hydroxy butyryl-CoA.

C) both acetyl-CoA and propionyl-CoA. D) palmitoyl-CoA.

E) propionyl-CoA.

5- Ketone bodies are formed in the liver and transported to the extrahepatic tissues mainly as:

A) acetoacetyl-CoA. B) acetone.

C) beta-hydroxybutyric acid. D) beta-hydroxybutyryl-CoA. E) lactic acid.

6- In comparing fatty acid biosynthesis with β oxidation of fatty acids, which of the following statements is incorrect?

A)

A thioester derivative of crotonic acid (trans-2-butenoic acid) is an intermediate in the synthetic path, but not in the degradative path.

B)

A thioester derivative of D-β-hydroxybutyrate is an intermediate in the synthetic path,

not in the degradative path.

C)

Fatty acid biosynthesis uses NADPH exclusively, whereas β oxidation uses NAD+

exclusively.

D)

Fatty acid degradation is catalyzed by cytosolic enzymes; fatty acid synthesis by mitochondrial enzymes.

E)

The condensation of two moles of acetyl-CoA in the presence of a crude extract is more rapid in bicarbonate buffer than in phosphate buffer at the same pH; the cleavage of acetoacetyl-CoA proceeds equally well in either buffer

7-The enzyme system for adding double bonds to saturated fatty acids requires all of the following except:

A)

a mixed-function oxidase.

B)

ATP.

C)

cytochrome b₅.

D)

molecular oxygen (O₂).

E)

NADPH.

8) The rate-limiting step in fatty acid synthesis is:

A)

condensation of acetyl-CoA and malonyl-CoA.

B)

formation of acetyl-CoA from acetate.

C)

formation of malonyl-CoA from malonate and coenzyme A.

D)

the reaction catalyzed by acetyl-CoA carboxylase.

E)

the reduction of the acetoacetyl group to a β-hydroxybutyryl group.

9- Which of the following occurs when cholesterol enters cells?

A) Cholesterol is released from LDL particles when the particles become internalized by lysosomes

B) LDL receptors on the cell surface recognize cholesterol in LDL particles.

C) The internalized LDL receptor is degraded to amino acids that can be recycled into new proteins

10 - Draw the four basic steps in the oxidation of a saturated fatty acid (the β-oxidation pathway). Show structures, name enzymes, and indicate where any cofactors participate.

11- Write a balanced equation for the β oxidation of palmitoyl-CoA, a 16-carbon, fully saturated fatty acid, and indicate how much of each product is formed.

Ans: The overall reaction is:

Palmitoyl-CoA + 7CoA-SH + 7FAD + 7NAD+ + 7H2O → 8 acetyl-CoA + 7FADH2 + 7NADH + 7H+

12- For each two-carbon increase in the length of a saturated fatty acid chain, how many additional moles of ATP can be formed upon complete oxidation of one mole of the fatty acid to CO₂ and H₂O?

Ans: Each —CH₂—CH₂— unit yields 14 extra ATP molecules. The two oxidations of the β-oxidation pathway produce 1 FADH₂ and 1 NADH, which yield 1.5 and 2.5 ATP,

respectively, by oxidative phosphorylation. The extra acetyl-CoA, when oxidized via the citric acid cycle, yields another 10 ATP equivalents: 3 NADH, 1 FADH₂, and 1 ATP or GTP.

13- What are ketone bodies and why do they form during fasting?

Ans: The ketone bodies, acetoacetate, β-hydroxybutyrate, and acetone, are overproduced during fasting, when fatty acids from stored triacylglycerols become the principle oxidizable fuel. Accumulation of acetyl-CoA and its precursor acetoacetyl-CoA favors ketone body formation. Because oxaloacetate is used for gluconeogenesis, it is withdrawn from the citric acid cycle, bringing that cycle to a near halt. The acetyl-CoA that is produced by β oxidation can no longer be oxidized via the citric acid cycle so it accumulates.

14- Fatty acid synthesis and fatty acid breakdown occur by similar pathways. Describe, very briefly, four ways in which the synthetic and breakdown pathways differ.

Ans: Fatty acid synthesis (in any order) (1) employs NADPH as reducing agent; (2) involves an acyl group bound to a protein, ACP; (3) takes place in the cytosol of animals; (4) involves the condensation of malonyl- and acetyl-groups; (5) involves the formation of the D-β-hydroxyacyl derivative. Fatty acid breakdown (1) employs NAD+ as electron acceptor; (2) involves acyl groups bound to coenzyme A; (3) occurs in the mitochondrial matrix; (4) does not involve malonyl-derivatives; (5) involves the L-stereoisomer of the β-hydroxyacyl derivative.

15- Show the reaction that limits the rate of cholesterol synthesis from acetate, indicating the role of any cofactors that participate.

16- What are plasma lipoproteins? What is their general role in mamm6alian metabolism?

Ans: Plasma lipoproteins are protein-lipid aggregates that circulate in the blood, carrying phospholipids, triacylglycerols, cholesterol, and cholesteryl esters from their points of synthesis or absorption to the tissues in which they will be used. The lipid/protein ratio, and therefore the density, of plasma lipoproteins varies, giving rise to particles separable by ultracentrifugation: HDL, LDL, VLDL, and chylomicrons, for example.

17- Describe (briefly) two classes of genetic defects in humans that could produce an elevated blood serum cholesterol level.

Ans: 1) Mutations in the LDL receptor result in the failure of cells to take up by receptor-mediated endocytosis the cholestrol in LDL; the resulting high level of LDL in the blood is characteristic of familial hypercholesterolemia. 2) Mutations in the ABC1 protein of HDL result in a failure of the HDL to take up cholesterol and remove it from the blood.

18- Why is it more efficient to store energy as lipid rather than as glycogen?

Ans: First, the energy yield per gram of lipid (about 38 kJ/g) is more than twice that for carbohydrate (about 17 kJ/g). Second, lipid is stored as anhydrous lipid droplets, but carbohydrates such as glycogen and starch are stored hydrated, and the water of hydration roughly triples the effective weight of the carbohydrate, reducing the energy yield to about 6 kJ/g.

19-Explain briefly why we require fats in our diets.

Ans: Dietary fats provide the linoleate and linolenate that we need (for eicosanoid synthesis) but cannot synthesize.

20- Describe the process by which cholesterol esters in the bloodstream enter cells.

Ans: The process is receptor-mediated endocytosis (described in Fig. 21-42, p. 825). LDL particles containing cholesterol esters interact via apoB-100 with specific LDL receptors in the cell surface, initiating endocytosis that brings the LDL into the cell within endosomes. Endosomes fuse with lysosomes, and lysosomal enzymes degrade the apoproteins;

cholesterol esters are released into the cytosol, and LDL receptors recirculate, reappearing on the cell surface.