Abstract
Fatty acids are important oxidative fuel for liver, kidney, skeletal muscle, and myocardium. There has been much interest in the role of fatty acids in the pathogenesis of non-insulin-dependent diabetes because they compete with glucose for oxygen and inhibit whole body glucose disposal via the 'Randle cycle,' Control of lipolysis in adipose tissue determines systemic fatty acid supply. A wide range of hormones and other substances have been recognized as regulators of lipolysis, but insulin and catecholamines appear to be the most important. The regulation of lipolysis, in most circumstances, provides a supply of lipid fuel exceeding the rate of lipid oxidation, requiring reesterification to triglyceride of surplus circulating free fatty acids. Thus, free fatty acid supply is usually not matched to the demand for lipid oxidation, and there is no known mechanism for accurately sensing such demand. This lax regulation may be disadvantageous in conditions such as aging, stress, obesity, and diabetes, where the antilipolytic effect of insulin is impaired and lipolysis is therefore increased. In these conditions, the surfeit of fatty acid may impair glucoregulation. In addition, the excess lipolysis may induce hypertriglyceridemia (via increased very low density lipoprotein production) and thus contribute to atherogenesis. Considerable additional research is needed in order to fully understand both normal lipolytic regulation and the abnormalities of lipolysis which accompany pathological conditions.
Highlights
THE RANGE O F LIPOLYTIC PROCESSESLipolysis refers to processes in which triglyceride is hydrolyzed, via di- and monoglyceride intermediates, to fatty acids and glycerol [1]
Adipose tissue lipolysis is the major regulator of the body’s supply of lipid energy because it controls the release of fatty acids (FA) into the plasma, where they circulate as free fatty acids (FFA) complexed to albumin [4]
This extracellular lipolysis is controlled by lipoprotein lipase (LPL, EC 3.1.1.34), an enzyme bound to the luminal side of the capillary endothelium and activated by circulating apolipoprotein C-I1 and inhibited by apolipoprotein C-I11 [16, 17]
Summary
Lipolysis refers to processes in which triglyceride is hydrolyzed, via di- and monoglyceride intermediates, to fatty acids and glycerol [1]. T h e intracellular TG in liver and muscle (both skeletal and myocardial) has a metabolic importance [3, 6] out of proportion to its small mass (0.2-0.5 kg in a healthy young adult) These stores serve as a buffer that compensates for short-term differences in FFA supply and lipid oxidative demand. The fatty acids transported into the cell as a result of this process may either be reesterified into TG (their predominant fate in adipose tissue) or immediately oxidized (more likely in skeletal muscle or myocardium) This extracellular lipolysis is controlled by lipoprotein lipase (LPL, EC 3.1.1.34), an enzyme bound to the luminal side of the capillary endothelium and activated by circulating apolipoprotein C-I1 and inhibited by apolipoprotein C-I11 [16, 17]. Much remains to be learned about the relationship between atherosclerosis and abnormalities of lipolysis, but it has been postulated that excess FFA flux has a proximal role in the atherogenic lipoprotein profile and increased vascular disease seen in obesity and NIDDM [54, 62]
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