Obesity and Lipoproteins
Excess body fat adversely affects plasma lipoproteins in humans (Brunzell, 1984). Specifically, obesity results in increased levels of very-low-density lipoproteins (VLDL) and low-density lipoproteins (LDL), which are considered atherogenic, and decreased levels of high-density lipoproteins (HDL), which are considered antiatherogenic (Wolf and Grundy, 1983). Turnover studies of apolipoprotein B, the main constituent of VLDL and LDL, have demonstrated overproduction of hepatic VLDL in obese subjects (Kesäniemi et al., 1985). Furthermore, increased plasma postheparin hepatic triglyceride lipase (HTGL) (Reitmann et al., 1982) and lecithin—cholesterol acyltransferase (LCAT) (Akanuma et al., 1973) activities have been reported. The inverse relationship between HTGL activity and HDL cholesterol levels substantiates the role of this enzyme in the metabolism of HDL (Kuuisi et al., 1980). LCAT contributes to the mobilization of cholesterol from peripheral cells by esterifying free cholesterol contained in HDL (Glomset, 1968). Since VLDL are preferred acceptors for cholesteryl ester (Eisenberg, 1985), one consequence of VLDL overproduction in obesity is thought to be the impairment of cholesterol mobilization (Wallentin and Angelin, 1978).
KeywordsLCAT Activity Hepatic Triglyceride Lipase Dipalmitoyl Lecithin Adipose Tissue Lipoprotein Lipase Activity HTGL Activity
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