Ketosis induction

Ketosis induction" refers to the process by which the body enters the metabolic state known as **ketosis**, characterized by elevated levels of circulating ketone bodies—primarily β-hydroxybutyrate, acetoacetate, and acetone. This occurs when carbohydrate intake is sufficiently restricted (<50 grams per day for most people) or during prolonged fasting/exercise so that glycogen stores are depleted. The liver then increases fatty acid oxidation and converts resulting acetyl-CoA into ketones via mitochondrial pathways. These ketones serve as alternative energy substrates for tissues including the brain when glucose availability is low. While "induction of ketosis" has therapeutic relevance—such as in ketogenic diets for epilepsy management or potential benefits in neurodegenerative/cardiovascular diseases—it does not represent a discrete molecular entity but rather describes a systemic physiological adaptation involving multiple enzymes, transporters, hormones (insulin/glucagon), and organs. Therefore, "ketosis induction" should **not be considered a canonical drug target**, receptor, enzyme, transporter etc.; it describes an induced *metabolic state* rather than any single molecule/protein/gene product.

Other names

KetosisKetosis inductionInduction of ketosisNutritional ketosis

Not applicable; "ketosis induction" is a physiological process/state rather than an actionable molecular target. Some drugs may induce this state indirectly by altering glucose handling or metabolism (e.g., SGLT2 inhibitors increase ketone body production by promoting glycosuria and shifting substrate utilization)