In the liver, what causes inadequate levels of oxaloacetate that affects the citric acid cycle?

In the liver, the process of gluconeogenesis leads to inadequate levels of oxaloacetate, which can significantly impact the citric acid cycle. During gluconeogenesis, the liver synthesizes glucose from non-carbohydrate sources, such as amino acids and glycerol. This process requires the conversion of pyruvate to oxaloacetate in order to eventually produce glucose. When gluconeogenesis is highly active, especially in conditions like fasting or low carbohydrate intake, the demand for oxaloacetate increases, which can deplete its availability for the citric acid cycle.

As oxaloacetate is a key substrate for the cycle, its shortage hampers the ability of the cycle to oxidize Acetyl CoA effectively, thereby reducing the overall production of ATP. In this context, the increased usage of oxaloacetate for gluconeogenesis leads to insufficient amounts remaining for the citric acid cycle when it is needed for energy production.

In summary, when gluconeogenesis is occurring at high rates, it can divert oxaloacetate away from the citric acid cycle, causing inadequate levels that negatively affect cellular respiration and energy production.