Postprandial dyslipidemia in insulin resistance: Mechanisms and role of intestinal insulin sensitivity

Chylomicrons: A Key Biomarker and Risk Factor for Cardiovascular Disease and for the Understanding of Obesity

“…In an animal model, proteins involved in the assembly of prechylomicron transport vesicles, which is the rate-limiting step in transportation of TG through the enterocyte, were increased in the insulin-resistant gut [61]. Moreover, in insulin-resistant states and T2DM, FFA plasma concentrations are increased and it was shown in vivo that a continuous intravenous infusion of FFA stimulates both intestinal and hepatic TRL production [66].…”

“…Besides delayed clearance of TRLs in obese subjects, emerging evidence also shows intestinal overproduction of chylomicrons as a major contributor of postprandial lipemia in insulin resistance [61]. In an animal model, proteins involved in the assembly of prechylomicron transport vesicles, which is the rate-limiting step in transportation of TG through the enterocyte, were increased in the insulin-resistant gut [61].…”

“…1) [59,60]. Another mechanism is the production of apoE-deficient chylomicrons in insulin resistance hampering the clearance of these aberrant chylomicrons [61]. This is also reflected by higher apoB48 concentrations in obese subjects compared to healthy subjects in both the fasted and the fed state, which can be measured easily with a novel enzymelinked immunosorbent assay (ELISA) [62].…”

Postprandial lipemia as an early predictor of cardiovascular complications in childhood obesity

“…53,54 The intestine is a major site of lipid synthesis in the body, and upregulated de novo lipogenesis may be the result of a number of factors: intestinal insulin resistance, enhanced dietary lipid absorption, and/or increased expression and activity of proteins involved in CM assembly and secretion. 55,56 Furthermore, for those individuals at risk for CVD, CM can be poorly hydrolyzed and their clearance via hepatic receptormediated pathways delayed. 14,15 The etiologic significance of delayed CM-remnant clearance is an increased propensity for these particles to become entrapped and accumulate within the intima of arterial vessels.…”

Combination of acarbose and ezetimibe prevents non-alcoholic fatty liver disease: A break of intestinal insulin resistance?

“…Thus, the upregulation of SREBP-2 under combination therapy of ezetimibe and acarbose can lead to remarkable changes in the acute postprandial and chronic secretion of different gastro-intestinal hormones. Based on the new mechanisms for the regulation of the rate of production of triglyceride-rich lipoproteins in the gut and the strong involvement of the gastro-intestinal hormones in this process [8], the intestinal effects on the drug combination studied are decisive for the observed prevention of NAFLD. Moreover, the modulation of gastro-intestinal hormone responses may explain a dramatic weight reduction observed under combination of acarbose and ezetimibe in this study.…”