In the liver, higher levels of NADH promote gluconeogenesis. I'm curious as to your thoughts on this claim.
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In the liver, higher levels of NADH promote gluconeogenesis. I'm curious as to your thoughts on this claim.
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- A higher concentration of NADH in the liver is associated with an increase in gluconeogenesis. Your thoughts on this assertion?Increased NADH concentrations in the liver encourage gluconeogenesis. What do you think about this assertion?Increased levels of NADH in the liver promote the process of gluconeogenesis. What do you make of this statement?
- NADH boosts gluconeogenesis in the liver. So, what do you think about this assertion?The production of glucose by the liver is facilitated by elevated amounts of the molecule NADH. What are your thoughts on the aforementioned assertion?Elevated levels of NADH in the liver promote gluconeogenesis. I'm curious as to your thoughts on this claim.
- After several days of starvation, the capacity of the liver to metabolize acetyl-CoA via the citric acid cycle is greatly diminished. Explain.CH3CH2OH + NAD+ --> CH3CHO + NADH +H+ Explain how this reaction inhibits the production of pyruvate from lactate. Why does this lead to low blood glucose levels? please and thank youThe enzyme that decarboxylates pyruvate before it gets converted to Acetyl CoA is a. Pyruvate dehydrogenase b. Pyruvate decarboxylase c. Pyruvate carboxylase d. Pyruvate oxidative decarboxylase
- Why does epinephrine stimulate glycolysis? I know why epinephrine stimulates glycogenolysis which is to release glucose stores. But epinephrine stimulating glycolysis seems counterintuitive as it would synthesize less glucose and more pyruvate?The same reactions that were seen in the process of converting pyruvate to acetyl-S-CoA, occur in step ____ of the citric acid cycle as ____________ is converted to _________________.How similar of an effect would a mutation in pyruvate dehydrogenase have, compared to a mutation in pyruvate carboxylase that blocks its ability to be regulated by acetyl-CoA?