The carboxylation of pyruvate by pyruvate carboxylase occurs at a very low rate unless acetyl-CoA, a positive allosteric modulator, is present. If you have just eaten a meal rich in fatty acids (triacylglycerols) but low in carbohydrates (glucose), how does this regulatory property shut down the oxidation of glucose to CO₂ and H₂O but increase the oxidation of acetyl-CoA derived from fatty acids?

The mechanism shut down the oxidation of glucose to CO2 and H2O but increases the oxidation of acetyl CoA derived from fatty acids by Tri carboxylic acid cycle.

Explanation:

When a person eat meal rich in fatty acid, the ingested fatty acid will undergo breakdown to form large amount of acetyl CoA. The so formed Acetyl CoA undergo oxidation by TCA cycle to generate CO2 and H2O.

on the other hand when a person has eaten a meal that is low in carbohydrates (glucose), at that time less glucose molecule will undergo glycolysis and oxidative de carboxylation to form less amount of acetyl CoA. The acetyl CoA accumulates rather than going further oxidation.

As the meal contain low amount of glucose after a certain period of time the glucose level will be depleted. So to maintain homeostasis of body glucose level the gluconeogenesis process is stimulated.

The conversion of pyruvate to oxaloacetate, one of the most important reaction of gluconeogenesis is boosted by the high cellular level of accumulated acetyl CoA.