Discuss the metabolic rationale for phosphorylation of acetyl-CoA carboxylase by AMP-activated protein kinase (AMPK) and cyclic AMP-dependent protein kinase (PKA).
Q: Briefly describe the biological rationale for each of the following allosteric phenomena: (a)…
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Q: Discuss the metabolic rationale for phosphorylation of acetyl-CoA carboxylase by AMP-activated…
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Q: Write the names of the reactions in which Acetyl CoA is obtained and used in metabolism and explain…
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Q: Describe the sources and fates of acetyl CoA
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Q: L What is the difference between the type of oxidation catalyzed by acyl-CoA dehydrogenase and that…
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Q: Compare the regulation of the pyruvate dehydrogenase complex in muscle and in liver.
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Q: Discuss how the isozymic forms of acetyl CoA carboxylase regulate fatty acid metabolism. Explain the…
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- Discuss the roles of phospholipase A2, cyclooxygenase, and lipooxygenase.Determine the specific types of mutations in the gene for the regulatory subunit of cyclic-AMP-dependent protein kinase (PKA) that could lead to either a permanently active PKA or a permanently inactive PKA.The serine residues in acetyl CoA carboxylase that are the target of the AMP-activated protein kinase are mutated to alanine. What is a likely consequence of this mutation?
- Describe the biochemical alterations that result in type 2 diabetes.Explain the indirect effect that allosteric effectors have on pyruvate dehydrogenase activity through phosphorylation/dephosphorylation of components within the PDH-complex.Propose specific types of mutations in the gene forthe regulatory subunit of cyclic-AMP-dependent proteinkinase (PKA) that could lead to either a permanently activePKA or a permanently inactive PKA.
- What is the metabolic significance of the following observations? (a) Only the liver form of pyruvate kinase is inhibited by alanine, and (b) only gluconeogenic tissues contain appreciable levels of glucose-6-phosphatase.Consider fructose-1,6-bisphosphatase (FBP) when responding to Parts A, B, and C. When writing your response, please put A, B, or C in front of the answer for each part. NOTE: Each part can be answered in 3-4 sentences.A. State the effect (inhibition OR activation) of insulin signaling on the activity of FBP. Explain why this effect makes sense and make sure you identify the pathway where FBP participates.B. In a type 2 diabetic liver cell, when the blood sugar level is high, will the activity of FBP be HIGHER, LOWER, or THE SAME AS the activity in a nondiabetic liver cell under the same conditions? Explain your reasoning.C. Now think about the insulin and glucagon signaling pathways that control activity of FBP. When a nondiabetic liver cell is exposed to low blood sugar, indicate one specific way the insulin or glucagon signaling pathway could be disrupted so that the activity of FBP is not controlled correctly. Then, explain the reasoning for your answer.Suggest what might be the actual cause of the various pathologies characterizing mevalonate kinase deficiency.
- The metabolic precursor for the production of most eicosanoids isSuggest the effects of each of the following mutations on the physiologicalrole of chymotrypsinogen:(a) R15S(b) C1S(c) T147SCompare the localization of GLUT4 with that of GLUT2 and GLUT3, and explain why these localizations are important in the response of muscle,adipose tissue, brain, and liver to insulin
