GLOSSARY

Monoglyceride Lipase (MGL) splits monoglycerides into glycerol and fatty acid.

Intracellular lipases and lipoprotein lipase differ in role and location. In the usual storage-lipolysis sequence, ATGL initiates triglyceride hydrolysis, HSL is especially active toward diglycerides and MGL completes monoglyceride hydrolysis. Lipoprotein lipase acts on circulating particle triglycerides. Fatty-acid release does not necessarily mean oxidation or net body-fat loss; utilization and re-esterification must also be considered before interpreting a lipolytic enzyme change as fat loss.

Lipolysis releases fatty acids and glycerol from triglycerides in adipose or intramuscular stores. Release differs from oxidation; some fatty acids are re-esterified. Greater mobilization or blood levels therefore do not prove net body-fat loss. Hormones, blood flow and tissue demand influence handling. Longer-term balance matters for body composition rather than assuming a lipolysis marker establishes that an exercise session or supplement burns more stored fat overall.

Lipid stores and turnover reflect entry, synthesis, breakdown and oxidation across tissues. Packaging, transport and re-esterification can accompany release. Mobilization, burning and net body-fat loss are therefore different reports. Athletes should assess body-composition trends alongside intake, performance and recovery. Maximizing momentary fat oxidation may overlook session fueling, and no isolated blood fatty-acid measure or pathway rate replaces a longer-term account of energy intake and use.