<Ul> <Li> The acetyl - CoA produced by beta oxidation enters the citric acid cycle in the mitochondrion by combining with oxaloacetate to form citrate . This results in the complete combustion of the acetyl - CoA to CO and water . The energy released in this process is captured in the form of 1 GTP and 11 ATP molecules per acetyl - CoA molecule oxidized . This is the fate of acetyl - CoA wherever beta oxidation of fatty acids occurs, except under certain circumstances in the liver . </Li> </Ul> <Li> The acetyl - CoA produced by beta oxidation enters the citric acid cycle in the mitochondrion by combining with oxaloacetate to form citrate . This results in the complete combustion of the acetyl - CoA to CO and water . The energy released in this process is captured in the form of 1 GTP and 11 ATP molecules per acetyl - CoA molecule oxidized . This is the fate of acetyl - CoA wherever beta oxidation of fatty acids occurs, except under certain circumstances in the liver . </Li> <P> In the liver oxaloacetate can be wholly or partially diverted into the gluconeogenic pathway during fasting, starvation, a low carbohydrate diet, prolonged strenuous exercise, and in uncontrolled type 1 diabetes mellitus . Under these circumstances oxaloacetate is hydrogenated to malate which is then removed from the mitochondrion to be converted into glucose in the cytoplasm of the liver cells, from where it is released into the blood . In the liver, therefore, oxaloacetate is unavailable for condensation with acetyl - CoA when significant gluconeogenesis has been stimulated by low (or absent) insulin and high glucagon concentrations in the blood . Under these circumstances acetyl - CoA is diverted to the formation of acetoacetate and beta - hydroxybutyrate . Acetoacetate, beta - hydroxybutyrate, and their spontaneous breakdown product, acetone, are frequently, but confusingly, known as ketone bodies (as they are not "bodies" at all, but water - soluble chemical substances). The ketone bodies are released by the liver into the blood . All cells with mitochondria can take ketone bodies up from the blood and reconvert them into acetyl - CoA, which can then be used as fuel in their citric acid cycles, as no other tissue can divert its oxaloacetate into the gluconeogenic pathway in the way that this can occur in the liver . Unlike free fatty acids, ketone bodies can cross the blood - brain barrier and are therefore available as fuel for the cells of the central nervous system, acting as a substitute for glucose, on which these cells normally survive . The occurrence of high levels of ketone bodies in the blood during starvation, a low carbohydrate diet, prolonged heavy exercise and uncontrolled type 1 diabetes mellitus is known as ketosis, and, in its extreme form, in out - of - control type 1 diabetes mellitus, as ketoacidosis . </P> <Dl> <Dd> The glycerol released by lipase action is phosphorylated by glycerol kinase in the liver (the only tissue in which this reaction can occur), and the resulting glycerol 3 - phosphate is oxidized to dihydroxyacetone phosphate . The glycolytic enzyme triose phosphate isomerase converts this compound to glyceraldehyde 3 - phosphate, which is oxidized via glycolysis, or converted to glucose via gluconeogenesis . </Dd> </Dl>

During starvation the acetyl coa coming from β–oxidation of fatty acids forms