Homework 11

The β-oxidation of myristyl-CoA (14:0) yields:

14 acetyl CoA + 12 FADH2 + 12 NADH + 12 H+.

7 acetyl CoA + 7 FAD + 7 NAD+

7 acetyl CoA + 7 FADH2 + 7 NADH + 7 H+.

6 acetyl CoA + 7 FADH2 + 7 NADH + 7 H+

7 acetyl CoA + 6 FADH2 + 6 NADH + 6 H+.

Epinephrine stimulates the mobilization of fatty acids and stimulates their accumulation as triacylglycerols.

Insulin stimulates fatty acid synthesis by activating acetyl CoA carboxylase 1.

Epinephrine stimulates AMPK, preventing the phosphorylation of acetyl CoA carboxylase 1.

Glucagon activates the carboxylase by enhancing the phosphorylation of AMPK.

Insulin stimulates the mobilization of fatty acids for oxidation

What are the conditions that lead to a "beer gut" due to the excess consumption of alcohol?

Excess ethanol metabolism leads to an accumulation of NADH that inhibits fatty acid metabolism.

NADH stimulates citric acid cycle enzymes that stimulates glucose-derived acetyl CoA metabolism.

NADH inhibits ketone body formation, stimulating glucose rather than fatty acid metabolism.

NADH produced from the metabolism of ethanol stimulates the citric acid cycle for glucose-derived acetyl CoA.

The processing of acetate in the liver becomes inefficient leading to a pH imbalance in liver cells, reducing enzyme efficiency in general.

Considering the final steps in cholesterol biosynthesis, when squalene is eventually converted to lanosterol, which of the following statements is correct?

Squalene is joined at carbons 1 and 30 to form the fused ring structure of sterols.

Squalene monooxygenase is considered a mixed function oxidase because it catalyzes a reaction in which only one of the oxygen atoms of O2 is incorporated into the organic substrate.

I Squalene monooxygenase uses reduced flavin nucleotides, such as FAD(2H), as the cosubstrate in the reaction.

All of the sterols have three fused rings (the steroid nucleus) and are alcohols with a hydroxyl group at carbon C3.

The action of squalene monooxygenase oxidizes C14 of the squalene chain, forming an epoxide.

Why do lipoprotein particles (e.g. VLDL) only have a monlayer of phospholipids instead of a typical lipid bilayer?

The phosphate of the lipids interact with the triglycerides and cholesterol esters of the particle.

The monolayer protects the particles from bile acids.

The acyl chains of the phospholipid monolayer interact with the triglycerides and cholesterol esters of the particle.

The monolayer blocks proteases from degrading the particle.

The glycerol backbone solubilizes the triglycerides.

Lovastatin is used to lower cholesterol by inhibiting the function of which protein?

Suppose 14C-labeled CO2 is used to form malonyl-CoA from acetyl-CoA. If this labeled malonyl-CoA is used for palmitate synthesis, which carbon atom(s) in the fatty acid would be radiolabeled?

Fatty acids are adenylated prior to reacting with Coenzyme A to make Acyl-CoA. What is the purpose of the adenylation?

This allows for the growth of acyl chain length.

Adenylation leads to the addition of ATP to acyl chains.

Adenylation prevents Acyl-CoA from interacting with Coenzyme A.

This creates a phospho-ester bond that can be "attacked" by Coenzyme A.

All of the above.

When fatty acid biosynthesis is stimulated, β-oxidation of fatty acids is inhibited. This inhibition occurs mainly because:

High levels of citrate stimulate acetyl-CoA synthase.

High levels of ATP inhibit phosphofructokinase.

Malonyl-CoA inhibits carnitine acyltransferase I.

Acetyl-CoA activates pyruvate carboxylase.

The pool of acetyl-CoA is depleted by the TCA cycle and fatty acid biosynthesis.

Homework 11

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