Department of Agriculture, Food, and Nutritional Science, 4-126 Li Ka Shing Centre for Research Innovation, University of Alberta, Edmonton, AB T6G OK2, Canada.
JPEN J Parenter Enteral Nutr. 2013 Jul;37(4):517-28. doi: 10.1177/0148607112467820. Epub 2012 Dec 5.
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.
快餐饮食引起的高胰岛素血症和脂质及脂蛋白代谢改变可能导致非酒精性脂肪肝(NAFLD)。我们假设,与健康儿童相比,富含饱和脂肪(SFA)的膳食会引起肥胖的 NAFLD 儿童餐后持续时间更长的脂血症和高胰岛素血症、增加炎症和改变脂蛋白表达。
我们前瞻性研究了 31 名儿童(NAFLD,13.1 ± 2.6 岁,n = 11;年龄匹配的肥胖,14.3 ± 1.7 岁,n = 9;瘦,13.6 ± 2.6 岁,n = 11)在食用高脂肪(18.8%)膳食后。在餐前和餐后 1、3 和 6 小时采集血液,用于分析丙氨酸转氨酶(ALT);天门冬氨酸转氨酶(AST);γ-谷氨酰转移酶;瘦素;C-反应蛋白;(空腹)胰岛素;葡萄糖;甘油三酯(TGs);总胆固醇、高密度脂蛋白和低密度脂蛋白胆固醇;脂联素;非酯化脂肪酸(NEFAs);炎症标志物(TNF-α、IL-6、IL-10);载脂蛋白 B48、B100 和 CIII;以及 TG 馏分的脂肪酸(FA)组成。
患有 NAFLD 的儿童空腹 ALT(87 ± 54 U/L)、AST(52 ± 33.5 U/L)和载脂蛋白-CIII(20.6 ± 11.3 mg/dL)水平显著升高,且餐后高胰岛素血症(iAUC 胰岛素:225 ± 207[NAFLD]比 113 ± 73[肥胖]比 47 ± 19.9[瘦]mU/L-h;P <.001);抑制 NEFA(iAUC-NEFA:1.7 ± 0.9[NAFLD]比 0.6 ± 0.3[肥胖]比 1 ± 0.7[瘦]mEq/L-h);以及餐后 3-6 小时载脂蛋白 B48 的升高,与肥胖和瘦对照组相比(P <.05)。
富含饱和脂肪的膳食会引起肥胖的 NAFLD 儿童和非肥胖儿童餐后血脂异常、高胰岛素血症和脂蛋白表达改变。