lipidmetabolizing

Lipid metabolism encompasses the biochemical pathways involved in the synthesis, modification, degradation, and disposal of lipids. The term lipid-metabolizing is a general descriptor for processes that degrade or transform lipids, releasing fatty acids and other components that can be used for energy, signaling, or biosynthesis. It includes lipolysis, fatty acid oxidation, and related pathways.

Lipolysis is the hydrolytic breakdown of triglycerides in adipose tissue and other stores, catalyzed by lipases such as adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), and monoacylglycerol lipase (MGL). Hormonal regulation is central: catecholamines and cortisol stimulate lipolysis via cAMP/PKA signaling, while insulin inhibits lipolysis by suppressing these pathways.

Free fatty acids released during lipolysis bind albumin in the bloodstream and are transported to tissues for oxidation or re-esterification. In mitochondria, beta-oxidation converts fatty acids to acetyl-CoA, generating NADH and FADH2 for ATP production. Transport into mitochondria requires the carnitine shuttle, notably CPT1; peroxisomal beta-oxidation also metabolizes very long-chain fatty acids.

Lipid mobilization intersects with lipoprotein metabolism: lipoprotein lipase (LPL) hydrolyzes triglycerides in chylomicrons and VLDL, releasing fatty acids for tissue uptake. Glycerol released during lipolysis can be used for gluconeogenesis in the liver or glycolysis in other tissues.

Regulation and clinical relevance: dysregulation of lipid-metabolizing pathways contributes to obesity, insulin resistance, and fatty liver disease. Inherited defects in lipases or fatty acid oxidation enzymes (for example, LPL deficiency or medium-chain acyl-CoA dehydrogenase deficiency) illustrate the physiological importance of these pathways.