Explain the biochemical consequences of Glucose-6-Phosphatase deficiency that results in gout due to increased production of Uric Acid.
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- Explain how genetic mutations of phosphoribosyl pyrophosphate synthetase causing superactivity lead to excessive uric acid production.hyperammonemia in patients is compounded by the reality of the normal regulatory controls in the urea cycle. Explain how increased GDH oxidative deamination activity will inhibit the urea cycle., which indicates AG for each glycolytic reac- tion under intracellular conditions. Assume that glyceraldehyde-3- phosphate dehydrogenase was inhibited with iodoacetic acid. Which glycolytic intermediate would you expect to accumulate most rapidly, and why?
- Glucokinase acts as a glucose sensor in hepatocytes (livercells), a- and b-cells in the pancreas, enterocytes (intestinalwall cells), and the hypothalamus (a control center in thebrain of numerous physiological processes). Explain whyglucokinase can perform this role.Many patients with glucose 6- phosphatase deficiency have high serum levels of urate. Hyperuricemia can be induced in normal people by the ingestion of alcohol or by strenuous exercise. Propose a common mechanism that accounts for these findings.The Vmax of muscle glycogen phosphorylase is much larger than that of the liver enzyme. Discuss the functional signifi cance of this phenomenon.
- The interconverison of DHAP and GAP greatly favors the formation of DHAP at equilibirum. Yet the conversion of DHAP by triose phosphate isomerase proceeds readily. Why?Dehydroascorbate is unstable at pH values greater than 6 anddecomposes to form tartrate and oxalate. Cells use GSH toreduce the loss of ascorbate. What is the reaction pathwayfor the regeneration of ascorbate?Explain why people with a deficiency of the enzyme glucose 6-phosphate dehydrogenase (G6PDH) suffer from hemolytic anemia
- Patients with a form of early-onset diabetes were found to carry a variety of mutations reducing the function of the glucokinase (GK) enzyme. These patients are heterozygous for one of the mutations, and thus show only partial rather than complete loss of GK activity. Answer the following questions about these patients. How would blood sugar lovolc likoly bo affoctod in CK nautatieThe peroxisomal enzyme b-ketoacyl–CoA-thiolase does notbind medium-chain acyl-CoA, in contrast to the analogousmitochondrial enzyme. Explain why this phenomenon is anadvantage to the cell.Explain why the symptoms of a partial defi ciency in a urea cycle enzyme can be attenuated by a low-protein diet.