Acetyl co A represents Fat component, since the major source is fatty acid oxidation. Acetyl co A is completely oxidized in the TCA cycle in the presence of oxaloacetate. Pyruvate is mainly used up for Anaplerotic reactions to compensate for oxaloacetate concentration. Thus without carbohydrates (Pyruvate), there would be no anaplerotic reactions to replenish the TCA-cycle components. With a diet of fats only, the acetyl CoA from fatty acid degradation would not get oxidized and build up due to non functioning of TCA cycle. Thus fats can burn only in the flame of carbohydrates.
Like glycolysis, much of the energy consumed is used in the irreversible steps of the process.
Six high-energy phosphate bonds are consumed: two from GTP and four from ATP. Furthermore, two molecules of NADH are required for the reduction of two molecules of 1,3-bisphosphoglycerate in the reaction catalyzed by glyceraldehyde 3-phosphate dehydrogenase. The oxidation of NADH causes the lack of production of 5 molecules of ATP that are synthesized when the electrons of the reduced coenzyme are used in oxidative phosphorylation.
Also these energetic considerations show that gluconeogenesis is not simply glycolysis in reverse, in which case it would require the consumption of two molecules of ATP, as shown by the overall glycolytic equation.
Global control of gluconeogenesis is mediated by glucagon ( released when blood glucose is low ); it triggers phosphorylation of enzymes and regulatory proteins by Protein Kinase A (a cyclic AMP regulated kinase) resulting in inhibition of glycolysis and stimulation of gluconeogenesis. Recent studies have shown that the absence of hepatic glucose production has no major effect on the control of fasting plasma glucose concentration. Compensatory induction of gluconeogenesis occurs in the kidneys and intestine, driven by glucagon , glucocorticoids , and acidosis.