Abstract 167: Dietary Medium-chain Triglyceride Supplementation Has No Effect on Apolipoprotein B-48 and Apolipoprotein B-100 Kinetics in Insulin-resistant Males

Medium-chain triglyceride (MCT) supplements are used by clinicians to treat patients with severe hypertriglyceridemia at risk for pancreatitis. However, the potential mechanisms underlying the triglyceride-lowering effects of MCT have not been thoroughly examined yet in human. This double-blind crossover study compared the impact of a 4-week supplementation with MCT oil 20 g/d vs corn oil 20 g/d on the intravascular kinetics of apolipoprotein (apo) B-48-containing triglyceride-rich lipoproteins (TRL) and apoB-100-containing VLDL as well as on the expression of key intestinal genes involved in lipid metabolism in 28 obese insulin-resistant males. In vivo kinetics of TRL apoB-48 and VLDL apoB-100 were assessed using a primed-constant infusion of L-[5,5,5-D3]leucine for 12h in the fed state. Expression of key intestinal genes involved in lipid metabolism was assessed in a subgroup of participants (n=16) by real-time PCR quantification in duodenal biopsy performed at the end of each phase of the supplementation in the fasted state. Compared with corn oil, MCT supplement had no significant effect on plasma lipoprotein profile and the TRL apoB-48 and VLDL apoB-100 kinetics. There were significant positive correlations at the end of the MCT supplementation between expression of SREBP-2 and expression of HNF-4α (r=0.51; P<0.05), HMGCoAR (r=0.75; P<0.001), ACAT-2 (r=0.51; P<0.05), NPC1L1 (r=0.66; P<0.05), ACS-1 (r=0.74; P<0.001), LDL receptor (r=0.67; P<0.05) and PCSK-9 (r=0.60; P<0.05) in intestinal tissue. However, MCT supplement had no significant impact on the expression of those key lipid and fatty acid regulation genes compared with corn oil. These data indicate that 4-week supplementation with MCT in obese insulin resistant men has no effect on TRL apoB-48 and VLDL apoB-100 kinetics and on the intestinal expression of genes involved in lipid and fatty acid metabolism.