<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>
<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>
during starvation the acetyl coa coming from β -- oxidation of fatty acids forms
during starvation the acetyl coa coming from β -- oxidation of fatty acids forms
ketone
ketone