Postprandial lipid and apolipoprotein responses following three consecutive meals associate with liver fat content in type 2 diabetes and the metabolic syndrome

ObjectiveLiver fat is associated with dyslipidemia following a fat load. Previous studies demonstrated that alimentary fat is temporarily retained within enterocytes and mobilized by subsequently ingested nutrients. As this potentially contributes to cumulative postprandial hyperlipidemia, we assessed postprandial lipoprotein changes and their association with liver fat following 3 consecutive meals during a 24 h period in males with type 2 diabetes, and men with the metabolic syndrome (MetS).MethodsPlasma lipids were measured in 14 type 2 diabetic, 14 MetS and 14 healthy age-matched males, following a standardized breakfast (t = 0 h), lunch (t = 4 h) and diner (t = 8 h). Blood samples were collected before and at t = 2, 4, 6, 8, 12, 16, 20 and 24 h following breakfast. Liver fat was measured by proton magnetic resonance spectroscopy.ResultsType 2 diabetic (mean age 55 (4.2) years; HbA1c 7.2 (1.1)%) and MetS men had similar BMI, waist, blood pressure and triglycerides. 24 h-AUC triglycerides, ApoB, and cholesterol-rich-remnants, but not ApoB-48, differed significantly among groups (calculated by ANOVA, all P < 0.05). Liver fat was independently associated with 24 h-AUC triglycerides, ApoB and cholesterol-rich-remnants (r = 0.57, P < 0.001, r = 0.38, P = 0.017; r = 0.48, P = 0.002, respectively), but not with 24 h-AUC ApoB-48 (r = 0.22, P = 0.18).ConclusionsIn type 2 diabetes and the MetS exposure to 3 consecutive meals produced exaggerated 24 h triglyceride, ApoB and cholesterol-rich-remnant concentrations, which were closely associated with liver fat. Instead, ApoB-48 peak was delayed in type 2 diabetes, but not related to liver fat. In addition to liver fat, other mechanisms, including local intestinal processes, determine atherogenic postprandial lipoprotein changes following 3 consecutive meals during 24 h.