MudPhud20XX

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I get that you get metabolic acidosis in alcoholics since NAD is used in both alcohol metabolism and and converting lactate to pyruvate. Kaplan explains that since NAD is used in both metabolisms, you end up with lactic acidosis. I get that. But why hypoglycemia?

Kaplan says to carry out gluconeogenesis, NAD is required by lactate dehydrogenase to oxidize lactate to pyruvate. I mean I get this too, but it's hard to believe this one step makes you vulnerable to hypoglycemia. Pyruvate can also come from alanine. I am just looking for a better explanation for hypoglycemia in alcoholics.

Many thanks in advance.
 

notbobtrustme

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nope, that's pretty much it. Alcoholics throw their NAD/NADH ratio so out of whack that they can't do gluconeogenesis for their body's needs.
 
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AnalisCanalis

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Shifted NAD+/NADH ratio shunts pyruvate to lactate and oxaloacetate to malate. This leads to inhibition of gluconeogenesis.
 
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Apoplexy__

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Goljan also really stresses that EtOH is a mitochondrial uncoupling agent, compromising ATP production. You may have learned that chronic alcoholics utilize the P450 system more in their metabolism of EtOH; this system pumps out free radicals which seem to hit the mitochondria pretty hard. One of the primary lesions to the mitochondria is increased membrane permeability --> H+ leaks --> ineffective ATP synthase.
 
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