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

Abstract

This article is available online at http://www.jlr.org 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 ( 2-6 ). Following a meal, dietary fat enters the circulation in the form of chylomicrons, TRL with apoB48. Effi cient 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 nonesterifi ed fatty acid (NEFA) by underlying adipocytes; and iii ) the utilization or storage of NEFA ( 3, 5 ). 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 ( 5 ). Accordingly, delayed plasma clearance of postprandial TRL by WAT is believed to increase the infl ux of dietary TRL remnants and NEFA into nonadipose peripheral tissues, including muscle, pancreas, and liver, inducing lipotoxicity and insulin resistance ( 6-8 ). In the liver, this also leads to increased synthesis and secretion of VLDL, which further reduces chylomicron clearance due to competitive binding to LPL ( 9-14 ). Altogether, this increases the plasma concentrations of apoB-lipoproteins, which is measured as plasma apoB and represents mostly LDL particles (>90%) ( 14-16 ). Dysfunctional WAT is thus Postprandial hypertriglyceridemia is an independent risk factor for cardiometabolic disease ( 1 ). Many factors have been implicated in the etiology of hyperlipidemia;

Association of Dyslipidemia and Glycated Haemoglobin in Gestational Diabetes Mellitus

“…Our study had shown highly correlation between hbA1c and lipids profiles in GDM groups [10] [12]. Which predominately increase levels of triglyceride production, free fatty acids and glucose.…”

WAT apoC-I secretion: role in delayed chylomicron clearance in vivo and ex vivo in WAT in obese subjects

“…Postprandial dietary fat metabolism was assessed as previously reported (14,29). In brief, subjects consumed a high-fat meal labeled with 13 C-triolein [glycerol tri(oleate-1- C-NEFA were measured over 0, 1, 2, 4, and 6 h using isotope ratio mass spectrometry (14,29).…”

“…Subjects' fasting WAT samples were collected by needle biopsy from the right hip (gynoid) area under local anesthesia (Xylocaine, 20 mg/ml; AstraZeneca) as previously described (14,29). WAT samples were cleaned and preincubated in 1 ml HBSS for 30 min to wash out products of cellular damage induced by the biopsy.…”

“…In brief, subjects consumed a high-fat meal labeled with 13 C-triolein [glycerol tri(oleate-1- C-NEFA were measured over 0, 1, 2, 4, and 6 h using isotope ratio mass spectrometry (14,29). The postprandial clearance rates of plasma total TG, 13 C-TG, and 13 C-NEFA were calculated as the area under the 6 h curve of the incremental increase above baseline levels of plasma lipids (iAUC 6hrs ).…”

“…Homeostatic model assessment of insulin resistance (HOMA-IR) was calculated according to Matthews et al (32). Lipoprotein cholesterol content and LDL diameter were measured by a polyacrylamide gel electrophoresis system (FDA-approved, Lipoprint system; Quantimetrix) (14,29).…”