Low density lipoprotein delays clearance of triglyceride-rich lipoprotein by human subcutaneous adipose tissue.

Delayed clearance of triglyceride-rich lipoprotein (TRL) by white adipose tissue (WAT) promotes hypertriglyceridemia and elevated apoB-lipoproteins, which are primarily in the form of LDL. This study examines whether LDL promotes delayed clearance of TRL by WAT. Following the ingestion of a (13)C-triolein-labeled high-fat meal, obese women with high plasma apoB (> median 0.93 g/l, N = 11, > 98% as IDL/LDL) had delayed clearance of postprandial (13)C-triglyceride and (13)C-NEFA over 6 h compared with controls. AUC6 h of plasma (13)C-triglyceride and (13)C-NEFA correlated with plasma apoB but not with LDL diameter or adipocyte area. There was no group difference in (13)C-triolein oxidation rate, which suggests lower (13)C-NEFA storage in peripheral tissue in women with high apoB. Ex vivo/in vitro plasma apoB correlated negatively with WAT (3)H-lipid following a 4 h incubation of women's WAT with synthetic (3)H-triolein-TRL. LDL-differentiated 3T3-L1 adipocytes had lower (3)H-TRL hydrolysis and (3)H-NEFA storage. Treatment of women's WAT with their own LDL decreased (3)H-TRL hydrolysis and (3)H-NEFA uptake. Finally, LDL, although not an LPL substrate, reduced LPL-mediated (3)H-TRL hydrolysis as did VLDL and HDL. Exposure to LDL decreases TRL clearance by human WAT ex vivo. This may promote production of apoB-lipoproteins and hypertriglyceridemia through a positive-feedback mechanism in vivo.