Fat metabolism/Ketogenesis

"Fat metabolism/ketogenesis" is **not a single molecule or receptor**, but rather refers to interconnected metabolic pathways. **Fat metabolism** encompasses the breakdown of triglycerides into free fatty acids and their subsequent oxidation for energy. **Ketogenesis** is the specific biochemical process by which the liver converts excess acetyl-CoA—derived from β‑oxidation of fatty acids—into ketone bodies (acetoacetate, β-hydroxybutyrate, and acetone), especially during periods of low carbohydrate availability such as fasting, starvation, or uncontrolled diabetes[1][2][3]. This process occurs primarily in hepatic mitochondria and is regulated by hormones including insulin and glucagon. Key enzymes involved include carnitine palmitoyltransferase 1 (CPT1), thiolase, HMG-CoA synthase, and HMG-CoA lyase[1][5]. The resulting ketone bodies serve as alternative energy substrates for extrahepatic tissues like brain, heart, and skeletal muscle when glucose is scarce. Dysregulation can lead to pathological states such as ketoacidosis or contribute to chronic diseases like MASLD/MASH through effects on lipid homeostasis[4]. Because "fat metabolism/ketogenesis" describes processes rather than a discrete molecular target suitable for drug binding or modulation like an enzyme or receptor would be considered in pharmacology—it should not be classified as a therapeutic target itself. Instead, individual enzymes within these pathways may serve as drug targets. If you are seeking structured information about specific molecules within this pathway—such as "3-hydroxy-3-methylglutaryl-CoA synthase 2" (HMGCS2) for hepatic ketogenesis—a more precise query naming that enzyme would yield canonical target data.

Other names

Fat metabolismKetogenesis