When the acetyl-CoA produced during -oxidation in the liver exceeds the capacity of the citric acid cycle, the excess acetyl-CoA is used to synthesize ketone bodies – acetone, acetoacetate, and -hydroxybutyrate. This occurs in severe, uncontrolled diabetes: because the tissues cannot use glucose, they instead oxidize large amounts of fatty acids. Although acetyl-CoA is not intrinsically toxic, the mitochondrion must divert the acetyl-CoA to ketone bodies. What problem would arise if acetyl-CoA were not converted to ketone bodies? How does the diversion to ketone bodies solve the problem?

There is a need to transform the accumulation of acetyl-CoA into the ketone bodies, as one knows that acetyl-CoA is both labile and possess an enormous amount of energy. Hence, acetyl-CoA due to its unstable characteristic is not ideal for circulation within the tissues, and at the same time, the compound acetyl-CoA does not possess the tendency to pass through the cell membrane.  

Due to these reasons, the conversion of acetyl-CoA into the ketone bodies is done, the ketone bodies also act as an alternative source of energy. The ketone bodies work as water-soluble correspondents of fatty acids. The production of ketone bodies generally takes place within the liver cells' mitochondrial matrix. The three forms of ketone bodies are beta-hydroxybutyrate, acetoacetate, and acetone.  

The production of ketone bodies by the liver cells helps the cells of the brain at the time of starvation, as the brain cannot use fatty acids as an energy source, as the fatty acids cannot pass through the blood-brain barrier.  

small, big, or no change could occur in the phenotype. it could cause something as simple as a cats ears to curl backwards or something as frighting as death. it could also occur in the protien-coding area and have an effect on that but no effect on the amino acids. what has to occur is a changing in the hox gene or the control gene.

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