GLOSSARY

HMG-CoA Lyase cleaves HMG-CoA to form acetoacetate.

Ketogenesis produces transportable ketone bodies, mainly in the liver from acetyl units, often increasing with low carbohydrate availability or fasting. It differs from their use elsewhere. Higher ketones do not necessarily prove an energy deficit or fat loss, especially after external intake. Athletes need goal-, task- and tolerance-based assessment rather than assuming a natural pathway makes every ketogenic diet or ketone supplement superior. Production, concentration and oxidation are different outcomes.

Mitochondrially equipped tissues can convert usable ketone bodies back toward acetyl-CoA for oxidation. Healthy adult liver is a major producer without the usual ketolytic route of consuming tissues; red cells lack mitochondria for oxidative ketone use. Production and use need not match instantaneously. Availability does not eliminate every glucose need or establish superior high-intensity performance. Tissue-specific handling and actual oxidation matter beyond a raised blood ketone concentration.

Acetoacetate, beta-hydroxybutyrate and acetone belong to the physiological ketone-body grouping, although beta-hydroxybutyrate is chemically a hydroxy acid. Their energy use and acetone's fate differ. Interconversion relates to redox conditions, and breath odor does not precisely quantify total fuel use. Specify compound and endogenous or ingested source in nutrition reports. The ketone label does not identify one formula or one guaranteed performance outcome across all preparations.