Question

1. In untreated Type 1 diabetes, the hepatocyte's citric acid cycle becomes overwhelmed with acetyl-CoA fr Map excessive fatty acid oxidation. Although the excess acetyl-CoA is not toxic, it must be diverted into the formation of ketone bodies: acetone, acetoacetate, and D-(hydroxybutyrate.

What problem would arise if the excess acetyl-CoA were not converted to ketone bodies?

 

How does the diversion to ketone bodies solve the problem?

The enzymes converting acetyl-CoA to acetoacetate liberate the CoA to be used in further fatty acid oxidation.

As acetoacetate is formed, acetyl groups are removed from acetyl carnitine, allowing additional fatty acids to enter the mitochondria.

Formation of acetoacetate from acetyl-CoA liberates a proton, lowering the pH to the optimum value for fatty acid oxidation.

One Of theket ne bodies Sh droxybutyrate relieves the acetyl-CoA inhibition of B-hydroxyacyl-CoA dehydrogenase.

Answer 1

Ans 1: fatty acid oxidation would stop when the CoA is bound as acetyl-CoA

The mitochondrial CoA pool is small, so two acetyl-CoA are converted to acetoacetyl-CoA + CoA. And in the liver,acetoacetyl-CoA is converted to the ketone bodies: acetoacetate, β-hydroxybutyrate, and acetone. Note that acetone is a minor component of the ketone bodies. Ketone bodies can be metabolized by non-hepatic tissues.

Ans 2: the enzyme converting acetyl-CoA to acetoacetate liberates the CoA to be used in further fatty acid oxidation.

There will be no alternate energy source if starvation were to occur. Then the brain muscle and heart would not get the energy needed that would usually come from glucose. The mitochondrial pool of CoA is small, CoA must be recycled from acetyl-CoA through the formation of ketone bodies. This allows the operation of the beta oxidation pathways, necessary for energy production.