Chapter 27

Stages of processing. What are the three stages of triacylglycerol utilization?

In its entirety. Write the complete reaction for fatty acid activation.

Activation fee. The reaction for the activation of fatty acids before degradation is (EQUATION CAN'T COPY) This reaction is quite favorable because the equivalent of two molecules of ATP is hydrolyzed. Explain why, from a biochemical bookkeeping point of view, the equivalent of two molecules of ATP is used despite the fact that the left side of the equation has only one molecule of ATP.

Like Simon and Garfunkel. Match each term with its description. (a) Triacylglycerol_________ (b) Perilipin_________ (c) Adipose triglyceride lipase_________ (d) Glucagon_________ (e) Acyl CoA synthetase_________ (f) Carnitine_________ (g) \(\beta\) -Oxidation pathway_________ (h) Enoyl CoA isomerase_________ (i) 2,4 -Dienoyl \(\operatorname{CoA}\) reductase_________ (j) Methylmalonyl CoA mutase_________ (k) Ketone body_________ 1\. The enzyme that initiates lipid degradation 2\. Activates fatty acids for degradation 3\. Converts a cis- \(\Delta^{3}\) double bond into a trans- \(\Delta^{2}\) double bond 4\. Reduces \(2,4-\) dienoyl intermediate to trans- \(\Delta^{3}\) -enoyl CoA 5\. Storage form of fats 6\. Required for entry into mitochondria 7\. Requires vitamin \(\mathrm{B}_{12}\) 8\. Acetoacetate 9\. Means by which fatty acids are degraded 10\. Stimulates lipolysis 11\. Lipid-droplet-associated protein

Proper sequence. Place the following list of reactions or relevant locations in the \(\beta\) oxidation of fatty acids in the proper order. (a) Reaction with carnitine (b) Fatty acid in the cytoplasm (c) Activation of fatty acid by joining to CoA (d) Hydration (e) NAD \(^{+}\) -linked oxidation (f) Thiolysis (g) Acyl CoA in mitochondrion (h) FAD-linked oxidation

Too tired to exercise. Explain why people with a hereditary deficiency of carnitine acyltransferase II have muscle weakness. Why are the symptoms more severe during fasting?

A phantom acetyl CoA? In the equation for fatty acid degradation shown here, only seven molecules of CoA are required to yield eight molecules of acetyl CoA. How is this difference possible? $$\begin{aligned} \text { Palmitoyl } \operatorname{Co} \mathrm{A}+& 7 \mathrm{FAD}+7 \mathrm{NAD}^{+} \\ &+7 \mathrm{CoA}+7 \mathrm{H}_{2} \mathrm{O} \longrightarrow \\ 8 \text { Acetyl } \mathrm{CoA}+& 7 \mathrm{FADH}_{2}+7 \mathrm{NADH}+7 \mathrm{H}^{+} \end{aligned}$$

Comparing yields. Compare the ATP yields from palmitic acid and palmitoleic acid.

Counting ATPs \(1 .\) What is the ATP yield for the complete oxidation of \(\mathrm{C}_{17}\) (heptadecanoic) fatty acid? Assume that the propionyl CoA ultimately yields oxaloacetate in the citric acid cycle.

The best storage form. Compare the ATP yield from the complete oxidation of glucose, a six-carbon carbohydrate, and hexanoic acid, a six-carbon fatty acid. Hexanoic acid is also called caproic acid and is responsible for the "aroma" of goats. Why are fats better fuels than carbohydrates?

From fatty acid to ketone body. Write a balanced equation for the conversion of stearate into acetoacetate.

An accurate adage. An old biochemistry adage is that fats burn in the flame of carbohydrates. What is the molecular basis of this adage?

Missing acyl CoA dehydrogenases. A number of genetic deficiencies in acyl CoA dehydrogenases have been described. A deficiency in acyl CoA dehydrogenase presents itself early in life or after a period of fasting. Symptoms include vomiting, lethargy, and, sometimes, coma. Not only are blood levels of glucose low (hypoglycemia), but also starvation-induced ketosis is absent. Provide a biochemical explanation for the last two observations.

Missing ingredient. Why are liver cells not capable of using ketone bodies as a fuel?

Finding triacylglycerols in all the wrong places. Insulindependent diabetes is often accompanied by high levels of triacylglycerols in the blood. Suggest a biochemical explanation for the high blood levels of triacylglycerols.

Leaner times might follow. Why can't animals convert fats into glucose? Why are plants capable of such a conversion?

Losing protein. What is the purpose of protein degradation during the initial stages of starvation?

After lipolysis. During fatty acid mobilization, glycerol is produced. This glycerol is not wasted. Write a balanced equation for the conversion of glycerol into pyruvate. What enzymes are required in addition to those of the glycolytic pathway?

Ill-advised diet. Suppose that, for some bizarre reason, you decided to exist on a diet of whale and seal blubber, exclusively. (a) How would a lack of carbohydrates affect your ability to utilize fats? (b) What would your breath smell like? (c) One of your best friends, after trying unsuccessfully to convince you to abandon this diet, makes you promise to consume a healthy dose of odd-chain fatty acids. Does your friend have your best interests at heart? Explain.

Sleight of hand. Animals cannot affect the net synthesis of glycogen from fatty acids. Yet, if animals are fed radioactive lipids \(\left(^{14} \mathrm{C}\right),\) over time, some radioactive glycogen appears. How is the appearance of radioactive glycogen possible in these animals?

Necessary diversion. When acetyl CoA produced by \(\beta\) -oxidation exceeds the capacity of the citric acid cycle, ketone bodies are produced. Although acetyl CoA is not toxic, mitochondria must divert acetyl CoA to ketone bodies to keep functioning. Explain why. What would happen if ketone bodies were not generated?

A hot diet. Tritium is a radioactive isotope of hydrogen and can be readily detected. Fully tritiated, six-carbon saturated fatty acid is administered to a rat, and a muscle biopsy of the rat is taken by concerned, sensitive, and discreet technical assistants. These assistants carefully isolate all of the acetyl CoA generated from the \(\beta\) oxidation of the radioactive fatty acid and remove the CoA to form acetate. What will be the overall tritium-to-carbon ratio of the isolated acetate?