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Unformatted text preview: Carbohydrate Practice Problems These lectures are spread over several chapters: Chapter Reading Chapter 11 11.1 and 11.2 Chapter 20 20.3, 20.4, and 20.5 Chapter 16 16.3 and 16.4 Chapter 21 all Problems (pp. 324-325) #12 and 14 (pp. 590-591) #10 (pp. 473-474) # 9 (b,c), 10, and 16 (pp. 615-616) 2, 3, 4, 7, 9, 10, 11 (a, c, d, and e), 12 1. Use your knowledge of biochemistry to explain why surcalose tastes sweeter than sugar and yet has "no calories." Sucralose has a higher affinity for "sweet taste receptors," G protein coupled receptors located in the taste sensory cells, thus is perceived to be sweeter. Humans do not have the necessary enzymes to digest sucralose, thus it cannot be converted into energy metabolites and has no dietary calories. 2. Pure cellulose is tough, fibrous and insoluble in water. Glycogen isolated from liver, which has a comparable molecule weight, is soluble in water. What are the biological advantages to each molecule's physical properties? The insoluble fibers formed by aggregation of cellulose are required for the structural role the molecule plays in plant biology. Glycogen is a storage molecule, and its solubility in water makes it readily available to meet energy needs. The polysaccharides have some similarities: both are polymers of D-glucose connected by (1->4) linkages. What structural features of the two molecules explain the observed physical differences? Glucose monomers in cellulose are linked by (1->4) glycosidic bonds, which allow the formation of long rigid chains. These chains can be further stabilized by hydrogen bonds, eventually aggregating into long insoluble fibers. Glucose monomers in glycogen are linked by (1->4) glycosidic bonds, which cause bends in the chain, preventing the formation of long fibers. Glycogen is highly-branched, leaving many hydroxyl groups exposed thus increasing the molecules solubility in water. 3. What explains the observation that people born with a deficiency in the enzyme glucose 6-phosphate dehydrogenase become clinically anemic if they have a diet rich in fava beans? Red blood cells need NADPH to keep glutathione in a reduced state and prevent oxidative damage. Glucose 6-phosophate dehydrogenase (G6PD) is required for the pentose phosphate pathway, which generates NADPH. If a person is deficient in G6PD, then they are more susceptible to this type of damage. Fava beans contain toxic oxidants and should be avoided by patients with G6PD deficiency, as they are likely to build up high levels of the oxidant in their red blood cells, which could lead to oxidative damage to the plasma membrane, and eventually hemolytic anemia. 4. Why does starvation lead to loss of muscle mass? Muscle proteins are broken down to amino acids, which are converted to Citrate cycle intermediates that can be metabolized to oxaloacetate. This pool of oxaloacetate is then used as a substrate for gluconeogenesis. 5. Gluconeogenesis and glycolysis are opposing pathways. In what way(s) are they similar and in what way(s) are they different? Similarities - both involve many of the same carbohydrate intermediates. - they share some of the same enzymatic reactions. - both are regulated by many of the same effector molecules. Differences - gluconeogenesis is primarily a liver pathway, glycolysis is in every cell. - gluconeogenesis requires ATP, glycolysis generates ATP. - regulatory effectors have opposite effects on these two pathways. 6. Avidin, a protein found in egg whites, binds to biotin so tightly that it inhibits enzymes that require biotin. The enzyme pyruvate carboxylase, which catalyzes the conversion of pyruvate to oxaloacetate using biotin as a coenzyme. How will high concentrations of avidin affect gluconeogenesis? Is there a way around this effect? Avidin will inhibit when pyruvate or lactate are the starting substrate because pyruvate carboxylase requires biotin. Gluconeogenesis will still occur when oxaloacetate is the starting substrate- therefore glucose can still be made from amino acids. 7. Fructose 1,6 bisphosphatase catalyzes the hydrolysis of fructose 1,6 bisphosphate to form fructose 6 phosphate during gluconeogenesis. Explain why the congenital disease fructose 1,6 bisphosphatase deficiency results in high levels of blood lactate. Gluconeogenesis is required to metabolize lactate to glucose. Lactate from muscle is exported to the blood and taken up in the liver and converted to glucose ( the Cori cycle). Patients with F16BP deficiency cannot make glucose through gluconeogesis, therefore lactate accumulates. 8. Explain the four cellular fates of glucose 6-phosphate (including the pathways involved). Give one example of how the metabolic fate of this molecule is determined. Glucose 6-phosphate can be converted to: 1. Glucose through gluconeogenesis (high energy charge in the liver) 2. Glycogen through glycogen synthesis (high energy charge) 3. Ribose or other pentose phosphates through the pentose phosphate pathway (low [NADP+] and substrate availability) 4. Pyruvate through glycolysis (low energy charge in many cells) 9. Why do glucose molecules produced by the glycogen phosphorylase reaction yield more ATP than dietary glucose? How many more ATPs? The product of the glycogen phosphorylase reaction is glucose-1-phosphate, which is isomerized to glucose-6-phosphate and metabolized by the glycolytic pathway. Since this bypasses the requirement for ATP hydrolysis (by hexokinase) in the first step of the pathway, 1 additional ATP is produced by a glycogen derived glucose unit (31 ATPs rather than 30 ATPs). 10. What effect does protein kinase A (PKA) activation have on glycogen metabolism with respect to glycogen synthase and glycogen phosphorylase activities? Does PKA activation increase or decrease the amount of stored glycogen in the body? Protein kinase A activation results in the phosphorylation and inactivation of glycogen synthase , and at the same time, the phosphorylation and activation of glycogen phosphorylase through the phosphorylation and activation of phosphorylase kinase. PKA activation results in decreased amounts of stored glycogen because glycogen synthase is inactivated and glycogen phosphorylase is activated. ...
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This note was uploaded on 05/06/2010 for the course BIOC 460 taught by Professor Ziegler during the Spring '07 term at Arizona.
- Spring '07