Unformatted text preview: Lipid Metabolism Problem Set Reading: Chapter 22 (all) Chapter 26 Sections 26.2, 26.3, and 26.4 Problems: 1, 6, 8, 9, 11, 17 (a and b) and 19 Problems Chapter 22: 6, 8, 11, and 19 (really good review for the final) Chapter 26: 7, 10 plus problem set Note: Reading and problems have been combined for oxidation and synthesis 1. What two properties make triacylglycerols more efficient metabolic energy storage molecules than glycogen? Fatty acids that make up triacylglycerols are more reduced than glucose monomers that make up glycogen. Triacylglycerols are not hydrated while glycogen is hydrated- therefore more metabolic energy can be stored per gram. 2. When energy charge and the concentration of oxaloacetate in the liver are both low, was is the fate of excess mitochondrial acetyl CoA? What metabolic conditions will bring this about? Excess acetyl CoA is converted to ketone bodies when OAA levels are limiting but energy requirements are high. Ketone bodies are produced as a result of starvation (or diabetes). 3. Canitine acyltransferase deficiency is characterized by hypoglycemia and a lack of ketone bodies in the plasma during starvation. Use your knowledge of lipid metabolism to explain this condition. Without carnitine acyltransferase, there is no fatty acid oxidation and no acetyl CoA is produced for ketone body formation. Hypoglycemia (low blood sugar) results from lack of ATP from fatty acid oxidation (acetyl CoA ---> citrate cycle ---> Ox Phos) which is needed to drive gluconeogenesis during starvation. 4. Suppose you treat cultured adipocytes with an inhibitor to camp phosphodiesterase. How would this affect the adipocytes response to epinephrine? The response of adipocytes would be much longer. Hormone sensitive lipase would remain stimulated and thus more triacylglycerides would be converted to glycerol and fatty acids. 5. Acetyl CoA Carboxylase exists in an inactive non-filamentous (protomer) form and an active filamentous form. Citrate binds preferentially to the filamentous form, while palmitolyl-CoA binds preferentially to the protomer Citrate stimulates fatty acid synthesis. By binding acetyl CoA carboxylase in the filamentous form, it drives the equilibrium in the direction of the filament formation. Palmitoyl CoA is the product of fatty acid synthesis, thus it inhibits acetyl CoA carboxylase. By binding to the protomer form it drives the equilibrium in favor of the inactive form. 6. De novo cholesterol synthesis is drastically reduced when a diet high in cholesterol is consumed. Use your knowledge of cholesterol biosynthesis to explain this observation. Dietary cholesterol is taken up by the liver, raising intracellular cholesterol concentrations. HMG-CoA reductase is inhibited by cholesterol and cholesterol derivatives- therefore less cholesterol is synthesized. 7. Explain the chemical characteristics that make bile salts effective biological detergents. Bile salts are derived from cholesterol and are amphipathic molecules, making them effective detergents. (nonfilamentous) form. Explain how this observation is consistent with the role of acetyl-CoA carboxylase in fatty acid synthesis. ...
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- Spring '07
- Biochemistry, fatty acid oxidation