What is the primary fate of acetyl CoA during prolonged starvation?

During prolonged starvation, the primary fate of acetyl CoA is its conversion to ketone bodies. In this state, the body experiences a significant decrease in glucose availability, primarily because glycogen stores are depleted and gluconeogenesis is limited.

With the body's reliance on fat stores for energy, fatty acids are mobilized and transported to the liver. In the liver, these fatty acids undergo beta-oxidation, producing acetyl CoA as a byproduct. Since carbohydrates are scarce, acetyl CoA cannot enter the citric acid cycle in sufficient quantities to meet the energy demands. Instead, it is converted into ketone bodies through a process called ketogenesis.

Ketone bodies, which include acetoacetate, β-hydroxybutyrate, and acetone, serve as an alternative fuel source for many tissues, especially the brain, during prolonged fasting or starvation. This shift is a crucial metabolic adaptation, allowing the body to conserve glucose and utilize fat-derived ketones to meet energy needs.

Other options are less relevant during starvation; acetyl CoA is typically not converted to amino acids or glucose, as those metabolic pathways are not active or are functionally limited in this state. Additionally, the synthesis of fatty acids is not