Ketones question in relation to diabetes

[Phloston]

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In alcoholism, NADH:NAD+ increases, so beta-hydroxybutyrate:acetoacetate increases. Understandable.

In diabetic ketoacidosis, the beta-hydroxybutyrate:acetoacetate is also increased. Why?

 

[Phloston]

Nevermind. I just figured it out.

The nicotinamide equilibrium is always NAD+ <---> NADH + H+.

So in diabetic ketoACIDosis, the H+, not NADH, therefore drives the reaction to create more beta-hydroxybutyrate.

 

[Belleza156]

How come in Alcoholic ketoacidosis there is a greater Beta-OHB acid:acetoacetate and in DKA there is a greater acetoacetate:Beta-OHB acid ratio?

I know the answer is because of the greater NADH: NAD+ ratio in alcoholics drives the balance towards beta-OHB , but I am not understanding why? Why doesn't the acetoacetate accumulate? Does is NADH a cofactor for one reaction but not the other?

 

[Phloston]

How come in Alcoholic ketoacidosis there is a greater Beta-OHB acid:acetoacetate and in DKA there is a greater acetoacetate:Beta-OHB acid ratio?

I know the answer is because of the greater NADH: NAD+ ratio in alcoholics drives the balance towards beta-OHB , but I am not understanding why? Why doesn't the acetoacetate accumulate? Does is NADH a cofactor for one reaction but not the other?

Beta-hydroxybutyrate + NAD+ <---> acetoacetate + NADH + H+

Beta-hydroxybutyrate is an alcohol, so NAD+ oxidizes it to acetoacetate, which is a ketone.

Alcohol AND DKA increase the beta-hydroxybutyrate to acetoacetate ratio.

In alcoholics, it's because increased NADH forces the reaction to the left. In DKA, increased H+ forces the reaction to the left.

I've also had a practice question somewhere that asked about how many acetyl-CoA are produced in ketogenesis, and it's two. Acetoacetate becomes 2 acetyl-CoA.