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 13C-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 13C-triglyceride and 13C-NEFA over 6 h compared with controls. AUC6 h of plasma 13C-triglyceride and 13C-NEFA correlated with plasma apoB but not with LDL diameter or adipocyte area. There was no group difference in 13C-triolein oxidation rate, which suggests lower 13C-NEFA storage in peripheral tissue in women with high apoB. Ex vivo/in vitro plasma apoB correlated negatively with WAT 3H-lipid following a 4 h incubation of women舗s WAT with synthetic 3H-triolein-TRL. LDL-differentiated 3T3-L1 adipocytes had lower 3H-TRL hydrolysis and 3H-NEFA storage. Treatment of women舗s WAT with their own LDL decreased 3H-TRL hydrolysis and 3H-NEFA uptake. Finally, LDL, although not an LPL substrate, reduced LPL-mediated 3H-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. 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 13C-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 13C-triglyceride and 13C-NEFA over 6 h compared with controls. AUC6 h of plasma 13C-triglyceride and 13C-NEFA correlated with plasma apoB but not with LDL diameter or adipocyte area. There was no group difference in 13C-triolein oxidation rate, which suggests lower 13C-NEFA storage in peripheral tissue in women with high apoB. Ex vivo/in vitro plasma apoB correlated negatively with WAT 3H-lipid following a 4 h incubation of women舗s WAT with synthetic 3H-triolein-TRL. LDL-differentiated 3T3-L1 adipocytes had lower 3H-TRL hydrolysis and 3H-NEFA storage. Treatment of women舗s WAT with their own LDL decreased 3H-TRL hydrolysis and 3H-NEFA uptake. Finally, LDL, although not an LPL substrate, reduced LPL-mediated 3H-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. Postprandial hypertriglyceridemia is an independent risk factor for cardiometabolic disease (1Nordestgaard B.G. Benn M. Schnohr P. Tybjaerg-Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women.JAMA. 2007; 298: 299-308Crossref PubMed Scopus (1607) Google Scholar). Many factors have been implicated in the etiology of hyperlipidemia; among the most common is reduced triglyceride-rich lipoprotein (TRL) clearance by peripheral tissue. White adipose tissue (WAT) is a major regulator of TRL clearance, particularly in the postprandial state (2Samra J.S. Clark M.L. Humphreys S.M. Macdonald I.A. Frayn K.N. Regulation of lipid metabolism in adipose tissue during early starvation.Am. J. Physiol. 1996; 271: E541-E546PubMed Google Scholar, 3Frayn K.N. Coppack S.W. Fielding B.A. Humphreys S.M. Coordinated regulation of hormone-sensitive lipase and lipoprotein lipase in human adipose tissue in vivo: implications for the control of fat storage and fat mobilization.Adv. 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Efficient clearance of chylomicrons by WAT requires three sequential steps: i) the hydrolysis of chylomicrons by endothelial lipoprotein lipase (LPL); ii) the uptake of LPL-generated nonesterified fatty acid (NEFA) by underlying adipocytes; and iii) the utilization or storage of NEFA (3Frayn K.N. Coppack S.W. Fielding B.A. Humphreys S.M. Coordinated regulation of hormone-sensitive lipase and lipoprotein lipase in human adipose tissue in vivo: implications for the control of fat storage and fat mobilization.Adv. Enzyme Regul. 1995; 35: 163-178Crossref PubMed Scopus (151) Google Scholar, 5Evans K. Burdge G.C. Wootton S.A. Clark M.L. Frayn K.N. Regulation of dietary fatty acid entrapment in subcutaneous adipose tissue and skeletal muscle.Diabetes. 2002; 51: 2684-2690Crossref PubMed Scopus (129) Google Scholar). Dietary TRL remnants and NEFA that are not cleared by peripheral tissue are then taken up by the liver for utilization and resecretion as VLDL (TRL with apoB100). Healthy WAT is able to respond promptly to postprandial signals, such as insulin increasing the hydrolysis of dietary TRL and the uptake and storage of generated NEFA, thus reestablishing the homeostasis in plasma lipids. The storage versus the release of TRL-generated NEFA in human subcutaneous WAT was reported to be almost absent in the fasting state, to increase to 100% 1 h after the ingestion of a meal, and to decrease to 10–30% 6 h after the meal (5Evans K. Burdge G.C. Wootton S.A. Clark M.L. Frayn K.N. Regulation of dietary fatty acid entrapment in subcutaneous adipose tissue and skeletal muscle.Diabetes. 2002; 51: 2684-2690Crossref PubMed Scopus (129) Google Scholar). Accordingly, delayed plasma clearance of postprandial TRL by WAT is believed to increase the influx of dietary TRL remnants and NEFA into nonadipose peripheral tissues, including muscle, pancreas, and liver, inducing lipotoxicity and insulin resistance (6Faraj M. Lu H.L. Cianflone K. 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The of WAT is 3T3-L1 for as M. A. Cianflone K. in lipoprotein lipase by increasing fatty acid in 2004; PubMed Scopus Google in the or of women舗s LDL with the of was and adipocytes and with the 3H-TRL for 4 and in LPL was as M. A. Cianflone K. in lipoprotein lipase by increasing fatty acid in 2004; PubMed Scopus Google Scholar). Cell was by release in the a M. A. Cianflone K. in lipoprotein lipase by increasing fatty acid in 2004; PubMed Scopus Google Scholar). The of N = 6 LDL is The of LDL WAT in LPL and uptake over 4 h was as but in the of own LDL The of three to WAT is reported for of the of LDL LPL LPL was following the of for and their incubation with for LPL was the 3H-TRL as M. A. Cianflone K. in lipoprotein lipase by increasing fatty acid in 2004; PubMed Scopus Google in the or of of The LDL and the of in women舗s fasting plasma to of apoB in and and VLDL as of LDL and and VLDL to the The of LPL into the over was also as the of a of LPL was over the 3H-TRL M. A. Cianflone K. in lipoprotein lipase by increasing fatty acid in 2004; PubMed Scopus Google in the or of of the as of N = 4 is WAT by the in in and into 4 was in a by The of adipocytes in of in three WAT is reported The three to of The adipocyte the of the the and a a over a are as over the 6 h by with was by by was by and 13C-NEFA was to the was and was and obese women plasma apoB median into of and high apoB. with high apoB had fasting plasma and and LDL diameter There no group in the and of the women = fat fat insulin NEFA diameter and for group difference by in a and for group difference by The oxidation versus circulation of the high-fat meal was in women over 6 with high apoB had delayed plasma clearance of and increase in the the 6 h of plasma versus versus = The had of NEFA with postprandial 1 and 2 of WAT There no group in postprandial plasma insulin or not to TRL of dietary women with high apoB also had delayed plasma clearance of 6 h versus versus = and AUC6 h of plasma versus versus = 13C-NEFA elevated the of the 6 h in the women with high to in women with apoB versus = was no group difference in the of 13C-NEFA oxidation this suggests uptake of 13C-NEFA for storage by peripheral tissue in women with high apoB. The of apoB-lipoproteins and compared in the of women In the fasting state, of plasma apoB and was in the TRL and with no group in TRL or TRL of apoB The group difference in plasma apoB was to in which of plasma apoB in with high apoB had fasting which an of apoB in In with the TRL and in the postprandial state and to a in women with high apoB. a major in the clearance of TRL and the of in TRL and with high apoB had TRL and in fasting (TRL = versus = versus and postprandial (TRL = versus = versus for of TRL TRL the group in the fasting = versus = not and the postprandial state = versus = not The increase in the of fasting TRL with in the postprandial state was in of the with was not as most of apoB is to LDL, which is in in in the apoB and of apoB correlated with h of plasma and fasting with TRL for fasting plasma correlated to h of plasma and fasting plasma to h of plasma that the of elevated remnants and postprandial TRL clearance be for by a correlated with the h of plasma and the of LDL with h of plasma for in this that women with high in the form of have delayed hydrolysis and clearance of postprandial dietary TRL by peripheral tissue reduced uptake of TRL remnants by the liver, in postprandial plasma and TRL in and obese women = h of and of the with also with in a and of the with also with whether WAT may to reduced dietary TRL clearance in women with high WAT for 4 h with synthetic and tissue 3H-lipid was in plasma apoB correlated negatively with WAT 3H-lipid = lower hydrolysis of 3H-TRL and uptake and storage of generated 3H-NEFA with plasma apoB. the of WAT 3H-lipid was with apoB = not with TRL apoB. a 3H-NEFA after the 3H-TRL for 4 h in the of WAT. The that 3H-NEFA was the of 3H-TRL of the WAT 3H-lipid was in the form of WAT of This suggests that to a high of a with TRL clearance and storage. that in 3T3-L1 in the or of elevated of LDL with LDL to as LDL-differentiated adipocytes compared with control adipocytes Following adipocyte incubation with 3H-TRL for 4 LDL-differentiated adipocytes had lower hydrolysis of 3H-TRL and uptake and storage of 3H-NEFA as lower 3H-lipid and in The of LDL was not to the in as the adipocytes was not by LDL over the of whether LDL may also have an WAT WAT for 4 h with synthetic 3H-TRL own LDL LDL was of LDL is not an LPL is in LPL PubMed Scopus Google Scholar). There no group in the of WAT to LDL the for of LDL WAT LDL of reduced 3H-TRL hydrolysis by whether in versus versus = or = LDL of whether in versus versus = or = the of reduced 3H-TRL hydrolysis and 3H-NEFA uptake with LDL LDL did not WAT 3H-lipid or with plasma apoB that was in not whether the of LDL 3H-TRL hydrolysis of WAT with in the or of women舗s own LDL LDL reduced the uptake of 3H-NEFA by whether as versus versus or = to the 3H-TRL was no of LDL WAT 3H-lipid versus versus = was no of adipocyte with WAT 3H-TRL or 3H-NEFA uptake the WAT with 3H-TRL or Finally, LDL is to to LPL M. M. K. J. P. of lipoprotein in of the for a of lipoprotein 2007; PubMed Scopus Google Scholar, J. A. M. P. of to lipoprotein lipase is but not Biol. 276: PubMed Scopus Google and reported to with LDL for to LPL J. A. M. P. of to lipoprotein lipase is but not Biol. 276: PubMed Scopus Google Scholar). This suggests that LDL may with 3H-TRL to this may not be as lipoprotein LPL in the or of women舗s LDL, and HDL. in for LDL, LPL compared with control LPL by This was for and LDL but not of VLDL LPL as to the LPL LPL LDL with and of of LPL as a of LPL a of and LDL, and There was a of LPL for VLDL and LDL LPL of and in this study that plasma clearance of dietary and NEFA is delayed in obese women with high plasma apoB difference in the oxidation of NEFA, which to reduced storage in peripheral tissue. the of WAT in postprandial TRL clearance, the of apoB-lipoproteins WAT of was ex and in vitro as i) plasma apoB was to in LPL and NEFA storage in women舗s WAT and ii) LDL-differentiated 3T3-L1 adipocytes had decreased in LPL and NEFA storage. In LDL had a TRL clearance as i) LDL of WAT for 4 h reduced the hydrolysis of synthetic TRL and the of NEFA, ii) LDL of WAT for 4 h reduced the uptake of NEFA, and iii) LDL LPL of the of this is to and of The of the to dietary fat a major as the to group in dietary NEFA have been had the been plasma NEFA, which is a of and NEFA with the of in not to be elevated apoB-lipoproteins and delayed TRL clearance, the that this in is not to whether elevated postprandial in was to reduced TRL hydrolysis by peripheral reduced uptake of TRL or the in vitro and ex an of LDL WAT an of LDL tissue be in to the liver, clearance of TRL and is by the of their of to LDL K. into factors lipoprotein PubMed Scopus Google Scholar). no group in the of TRL with elevated of LDL may have clearance by to the LDL This is by elevated fasting plasma in women with high apoB. and of LDL in this study an of LDL TRL clearance by human WAT. 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