A meal high in saturated fat evokes postprandial dyslipemia, hyperinsulinemia, and altered lipoprotein expression in obese children with and without nonalcoholic fatty liver disease.

Background: 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.

Methods: 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.

Results: 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).

Conclusions: A meal high in saturated fat evokes postprandial dyslipemia, hyperinsulinemia, and altered lipoprotein expression in obese children with and without NAFLD.