A meal high in saturated fat evokes postprandial dyslipemia, hyperinsulinemia, and altered lipoprotein expression in obese children with and without nonalcoholic fatty liver disease.JPEN J Parenter Enteral Nutr 2013; 37(4):517-28JJ
Hyperinsulinemia and altered lipid and lipoprotein metabolism induced by fast-food diets may contribute to nonalcoholic fatty liver disease (NAFLD). We hypothesized that a high saturated fat (SFA) meal would evoke prolonged postprandial lipemia and hyperinsulinemia, increased inflammation, and altered lipoprotein expression in obese children with NAFLD when compared with healthy children.
We prospectively studied 31 children (NAFLD, 13.1 ± 2.6 years, n = 11; age-matched obese, 14.3 ± 1.7 years, n = 9; lean, 13.6 ± 2.6 years, n = 11) following consumption of a high SFA (18.8%) meal. Prior to and at 1, 3, and 6 hours after meal consumption, blood was collected for analysis of alanine aminotransferase (ALT); aspartate aminotransferase (AST); γ-glutamyltransferase; leptin; C-reactive protein; (fasting) insulin; glucose; triglycerides (TGs); total, high-density lipoprotein, and low-density lipoprotein cholesterol; adiponectin; nonesterified fatty acids (NEFAs); inflammatory markers (TNF-α, IL-6, IL-10); apolipoproteins-B48, B100, and CIII; and fatty acid (FA) composition of TG fractions.
Children with NAFLD had significantly higher fasting levels of ALT (87 ± 54 U/L), AST (52 ± 33.5 U/L), and apolipoprotein-CIII (20.6 ± 11.3 mg/dL) with postprandial hyperinsulinemia (iAUC insulin: 225 ± 207 [NAFLD] vs 113 ± 73 [obese] vs 47 ± 19.9 [lean] mU/L-h; P < .001); suppression of NEFA (iAUC-NEFA: 1.7 ± 0.9 [NAFLD] vs 0.6 ± 0.3 [obese] vs 1 ± 0.7 [lean] mEq/L-h); and prolonged elevations in apolipoprotein-B48 3-6 hours after meal consumption when compared with obese and lean controls (P < .05).
A meal high in saturated fat evokes postprandial dyslipemia, hyperinsulinemia, and altered lipoprotein expression in obese children with and without NAFLD.