Gluconeogenesis in fasting state is stimulated by:
High-Yield Explanation
Ans. b. Activation of pyruvate carboxylase by acetyl Co-A (Ref: Harper 29/e p190, 28/e p165: Lippincott 5/e p117)Gluconeogenesis in fasting state is stimulated by activation of pyruvate carboxylase by acetyl Co-A.Regulation of Gluconeogenesis:Glucagon stimulates gluconeogenesis by following three mechanisms:Decreasing level of fructose-2, 6-bisphosphate. which is inhibitor of fructose-1, 6-bisphosphatase enzyme, thus. In turn stimulating the gluconeogenesis.Glucagon elevates the level of cAMP, which pbospborylates pyruvate kinase and thus inactivates it, shunting PEP to gluconeogenesis.Glucagon increases the transcription of PEP carboxykinase gene and thus stimulates gluconeogenesis.Substrate availabilityAllosteric activation by acetyl Co-A: Acetyl Co-A derived from fatty acid oxidation inhibits pyruvate dehydrogenase (PDH) enzyme and simultaneously stimulates pyruvate carboxylase, thus shunting pyruvate to gluconeogenesis.Allosteric inhibition by AMP Regulatory and Adaptive Enzymes Associated with Gluconeogenesis InducerRepressorActivatorInhibitorPyruvate carboxylaseGlucocorticoids, glucagon, epinephrineQInsulinQAcetyl CoAQADPQPhosphoenol pyruvate carboxy kinaseGlucocorticoids, glucagon, epinephrineQInsulinQGlucagon? Glucose 6-phosphataseGlucocorticoids, glucagon, epinephrineQInsulinQ