This might be a stupid question, but i cant seem to figure this out. I understand that consume alcohol would increase NADH/NAD+ ration, which interm can effect two things and lead to lactic acidosis and fasting hypoglycemia.
lactic acidosis is due increase of Pyruvate convert to lactate via Lactate Dehydrogenase.
fasting hypoglycemia due to decrease of gluconeogensis via OAA become malate due to increase NADH/NAD+ ration, this would shunt away from gluconeogenesis. Here is my question: Gluconeogensis OAA---->Malate mitochondria and malate via shuttle to come out cytoplasm become PEP. So my question is if high NADH ratio would reverse this pathway, wouldnt this make more malate? Which meaning that there more gluconeogenesis occuring? Why then alcoholics still have coma due to fasting hypoglycemia? Thanks folks for your answer in advance.

yes it makes more malate, but only oxaloacetate can go up to phosphoenolpyruvate in gluconeogenesis. malate cannot do it.

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M.D., PGY-1
Internal Medicine / future interests - Infectious Diseases Fellowship

Isnt malate from mitochondria will use the malate shuttle to go out to cytoplasm, then convert to OAA? So if you have an accumlation of Malate in the mitochondria why wouldnt you have extra malate on the outside via the shuttle, and then why wouldnt it be convert to OAA. That is what i confuse on.