4. How does compromised pyruvate kinase activity lead to anemia ?
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- 2. A 4-year-old girl was diagnosed with thiamine deficiency and the symptoms include tachycardia, vomiting, convulsions. Laboratory examinations reveal high levels of pyruvate, lactate and a-ketoglutarate. Explain which coenzyme is formed from vitamin B, and its role in oxidative decarboxylation of pyruvate. For that: a) describe the structure of pyruvate dehydrogenase complex (PDH) and the cofactors that it requires; b) discuss the symptoms which are connected with the thiamine deficiency and its effects on PDH and a-ketoglutarate dehydrogenase complex; c) explain the changes in the levels of mentioned metabolites in the blood; d) name the deseribed discase,7. Explain the differences between Glycogenolysis in muscle and liver.5. Reciprocal regulation of glycogen phosphorylase and glycogen synthase activity.
- 1. There are two metabolic routes for the conversion of oxaloacetate to phosphoenolpyruvate (PEP). What factors likely indicate which route is used? Do the two routes have different requirements for cellular energy (e.g. ATP)? 2. Compare the export of glucose from hepatocytes to the import into hepatocytes. 3. Would you expect anaplerotic reactions to be active in the postprandial hepatocyte? Why?How does compromised pyruvate kinase activity lead to anemia?5. When the acetyl-CoA produced during B-oxidation in the liver exceeds the capacity of the citric acid cycle, the excess acetyl-CoA forms ketone bodies-acetone, acetoacetate, and D-b-hydroxybutyrate. This occurs in severe, uncontrolled diabetes: because the tissues cannot use glucose, they oxidize large amounts of fatty acids instead. Although acetyl-CoA is not toxic, the mitochondrion must divert the acetyl-CoA to ketone bodies. What problem would arise if acetyl-CoA were not converted to ketone bodies? How does the diversion to ketone bodies solve the problem?
- 13. What is the consequence of complete inhibition of all mutases in liver cells? A. Liver cannot provide free glucose to maintain blood glucose levels B. Glycogen synthesis is disrupted C. Glycerol cannot be converted to glucose D. The only fate of glucose-6-phosphate is to be converted to fructose-6-phosphate3. Which tissues can synthesize glucose through the gluconeogenesis pathway? Explain the reason.5. Which of the following enzymes is NOT used when fructose is metabolized to pyruvate in the liver? a. triose phosphate isomerase b. glyceraldehyde-3-phospate dehydrogenase c. glucokinase d. phosphofructokinase-1 e. pyruvate kinase
- What are the current treatments for Pyruvate Kinase Deficiency (PKD) patients?4. Which of the following statements regarding the coordinated regulation of glycolysis and gluconeogenesis is not true? A. Phosphofructokinase-1 (PFK-1) and fructose-1,6-bisphosphatase (FBPase-1) are reciprocally regulated. B. Activating PFK-1 leads to more glycolysis. C. Inhibiting FBPase-1 slows gluconeogenesis. D. Fructose-1,6-bisphosphate is the primary regulator of PFK-1 and FBPase-1. E. ATP inhibits PFK-1.8. Hypercholesterolemia is a frequent complication of diabetes mellitus in patients with prolonged hyperglycemia. Why a high level of glucose in blood causes hypercholesterolemia and atherosclerosis? For the answer explain: a) how glucose can interact with the proteins and the consequences of this reaction for the proteins; b) glycation of which proteins results in hypercholesterolemia; c) possible causes and complications of hypercholesterolemia.