Figure 36-1. The metabolic flow during the fed state. Increased blood glucose
triggers release of insulin and a decrease in the release of glucagon and lipoly-
tic hormones.
prompting the use of amino acid carbon skeletons from protein breakdown
for new glucose formation. The energy required for gluconeogenesis is
derived by increasing ß-oxidation of fatty acids mobilized from adipose stor-
age sites. Fatty acid synthesis is simultaneously inhibited to prevent a futile
cycle. As the tricarboxylic acid cycle’s supply of four-carbon intermediates in
liver mitochondria is drained for gluconeogenesis, rapid ß-oxidation of fatty
acids produces acetyl-CoA faster than the tricarboxylic acid cycle can metab-
olize the carbon atoms of acetyl-CoA to CO2 and free CoA. The result is a high
ratio of acetyl-CoA to free CoA and thus a slowing of ß-oxidation and com-
promise of liver mitochondrial ATP formation. The conversion of the free CoA
pool to acetyl-CoA is reversed by the formation of the ketone body acetoac-
etate (and later its reduced product, ß-hydroxybutyrate) regenerating free
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