Gluconeogenesis starvation state

Increased fatty acid oxidation is a characteristic of starvation and of diabetes meUims, leading to ketone body production by the Ever (ketosis). Ketone bodies are acidic and when produced in excess over long periods, as in diabetes, cause ketoacidosis, which is ultimately fatal. Because gluconeogenesis is dependent upon fatty acid oxidation, any impairment in fatty acid oxidation leads to hypoglycemia. This occurs in various states of carnitine deficiency or deficiency of essential enzymes in fatty acid oxidation, eg, carnitine palmitoyltransferase, or inhibition of fatty acid oxidation by poisons, eg, hypoglycin. 

In the normal fed state, pyruvate is oxidized via the pyruvate dehydrogenase complex (PDH), but in starvation. PDH is inactivated thus, pyruvate is converted into alanine (Fig. 15-16) which enters the blood and is conveyed to the liver, where gluconeogenesis takes place. 

Figure 16.30. Reciprocal Regulation of Gluconeogenesis and Glycolysis in the Liver. The level of fructose 2,6-bisphosphate is high in the fed state and low in starvation. Another important control is the inhibition of pyruvate kinase by phosphorylation during starvation.

It would be incorrect to assume that the changes described above follow a reproducible chronological pattern. While the production of ketone bodies is associated with starvation, it is possible that ketone body formation occurs much earlier. Similarly, processes such as gluconeogenesis occur even in the fed state, but the net contribution of these pathways becomes more important as starvation progresses. 

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