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Answer Key for Chem 365 Problem Set 10: Ketone Bodies and Fatty Acid Metabolism, Assignments of Biochemistry

The answers for problem set 10 of chem 365, covering topics on ketone bodies formation, atp production during metabolism, and fatty acid synthesis. It explains the role of ketone bodies as fuel sources during starvation and insulin deficiency, the process of forming complex lipids and unsaturated fatty acids, and the importance of carnitine in transporting fatty acids for oxidation.

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Pre 2010

Uploaded on 07/30/2009

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Chem 365
Problem set 10 answer key
1. Ketone bodies are formed primarily in the liver in the mitochondria. Ketone bodies are formed from the
condensation of 2 molecules of acetyl CoA to form acetoacetic acid (a ketone body). The acetoacetic
acid can be converted to β-hydoxybutyrate (another ketone body) by the enzyme β-hydroxybutyrate
dehydrogenase in the mitochondria of the liver if there is a large amount of NADH present in the liver
(high energy conditions).
Ketone bodies serve as a fuel for cardiac and skeletal muscles, as well as the central nervous system,
during starvation and insulin deficiency when glucose is in short supply. The muscles and central
nervous system must continue to operate even when starving, so more and more ketone bodies are
present in the blood which can lead to ketoacidosis over time. Ketoacidosis is fatal if not corrected in
time.
2. a) 0 ATP
b) 0 ATP
c) 129 ATP (all occurs in mitochondria so do not need to shuttle NADH across mitochondria)
d) 0 ATP
3. a) 214 ATP
b) 142 ATP
4. 1) formation of complex lipids for cell structure, 2) formation of prostaglandins and steroids, 3) as an
energy source
5. a) First the body synthesizes palmitic acid:
8 acetyl-CoA + 7 ATP + 14 NADPH + 14 H+ palmitic acid + 14 NADP+ + 8 CoA + 6 H2O + 7 ADP + 7 Pi
using the enzyme fatty acid synthase
b) The body then elongates the palmitic acid using 1 molecule of malonyl-CoA (which is made from
acetyl-CoA and 1 ATP molecules).
c) Finally the body desaturates the stearic acid to form oleic acid:
Stearic acid + NADPH + H+ + O2 oleic acid + NADP+ + 2H2O
6. To reduce acetoacetic acid to β-hyroxybutyrate requires NADH and H+. Therefore, the ratio of
acetoacetic acid/β-hyroxybutyrate depends on the NAD+/NADH ratio in the mitochondria. The
NAD+/NADH ratio is an indicator of the metabolic state of an individual.
7. Linoleic acid (18:2(9,12)) is an essential acid because it contains a double bond at position 12 which is
only 6 away from the terminal methyl group. The desaturase enzyme which is used to convert palmitic
to other unsaturated fatty acids can not create a double bond on the last 6 carbons in any fatty acid chain.
Therefore, the enzyme can not create a double bond at position 12, so the body can not synthesize
linoleic acid, and it becomes “essential” that you obtain this fatty acid through the diet.
8. A) Carnitine is required to transport fatty acyl CoA into the mitochondrial matrix for β oxidation. The
inhibition of fatty acid transport caused by a deficiency in carnitine diminishes energy production from
fats for muscular work. Excess fatty acyl-CoA can be converted to triaclglycerols in the muscle cells.
b) Since carnitine is not required to transport pyruvate, a product of glycolysis, into mitochondria for
oxidation, muscle glycogen metabolism is not affected in individuals with a carnitine deficiency.
9.

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Chem 365 Problem set 10 answer key

  1. Ketone bodies are formed primarily in the liver in the mitochondria. Ketone bodies are formed from the condensation of 2 molecules of acetyl CoA to form acetoacetic acid (a ketone body). The acetoacetic acid can be converted to β-hydoxybutyrate (another ketone body) by the enzyme β-hydroxybutyrate dehydrogenase in the mitochondria of the liver if there is a large amount of NADH present in the liver (high energy conditions).

Ketone bodies serve as a fuel for cardiac and skeletal muscles, as well as the central nervous system, during starvation and insulin deficiency when glucose is in short supply. The muscles and central nervous system must continue to operate even when starving, so more and more ketone bodies are present in the blood which can lead to ketoacidosis over time. Ketoacidosis is fatal if not corrected in time.

  1. a) 0 ATP b) 0 ATP c) 129 ATP (all occurs in mitochondria so do not need to shuttle NADH across mitochondria) d) 0 ATP

  2. a) 214 ATP b) 142 ATP

    1. formation of complex lipids for cell structure, 2) formation of prostaglandins and steroids, 3) as an energy source
  3. a) First the body synthesizes palmitic acid: 8 acetyl-CoA + 7 ATP + 14 NADPH + 14 H+ → palmitic acid + 14 NADP+ + 8 CoA + 6 H 2 O + 7 ADP + 7 Pi using the enzyme fatty acid synthase b) The body then elongates the palmitic acid using 1 molecule of malonyl-CoA (which is made from acetyl-CoA and 1 ATP molecules). c) Finally the body desaturates the stearic acid to form oleic acid: Stearic acid + NADPH + H+ + O 2 → oleic acid + NADP+ + 2H 2 O

  4. To reduce acetoacetic acid to β-hyroxybutyrate requires NADH and H+. Therefore, the ratio of acetoacetic acid/β-hyroxybutyrate depends on the NAD+/NADH ratio in the mitochondria. The NAD+/NADH ratio is an indicator of the metabolic state of an individual.

  5. Linoleic acid (18:2(9,12)) is an essential acid because it contains a double bond at position 12 which is only 6 away from the terminal methyl group. The desaturase enzyme which is used to convert palmitic to other unsaturated fatty acids can not create a double bond on the last 6 carbons in any fatty acid chain. Therefore, the enzyme can not create a double bond at position 12, so the body can not synthesize linoleic acid, and it becomes “essential” that you obtain this fatty acid through the diet.

  6. A) Carnitine is required to transport fatty acyl CoA into the mitochondrial matrix for β oxidation. The inhibition of fatty acid transport caused by a deficiency in carnitine diminishes energy production from fats for muscular work. Excess fatty acyl-CoA can be converted to triaclglycerols in the muscle cells. b) Since carnitine is not required to transport pyruvate, a product of glycolysis, into mitochondria for oxidation, muscle glycogen metabolism is not affected in individuals with a carnitine deficiency.