Hodson Leanne, Bickerton Alex S T, McQuaid Siobhán E, Roberts Rachel, Karpe Fredrik, Frayn Keith N, Fielding Barbara A
Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, OX3 7LJ, UK.
Diabetes. 2007 Oct;56(10):2433-41. doi: 10.2337/db07-0654. Epub 2007 Jun 29.
We aimed to determine differences in the postprandial contributions of different fatty acid sources to VLDL triglycerides (TGs) in healthy men and women with varying degrees of insulin resistance.
Insulin-resistant (n = 11) and insulin-sensitive (n = 11) men and women (n = 6) were given an intravenous infusion of [(2)H(2)]palmitic acid to investigate systemic nonesterified fatty acid (NEFA) incorporation into VLDL TGs. Participants were also fed a mixed meal containing [U-(13)C]palmitic acid to investigate the contribution of dietary fatty acids to VLDL TG production. Blood samples were taken over the following 6 h. Separation of VLDL was performed by density gradient ultracentrifugation and immunoaffinity techniques specific to apolipoprotein B-100.
Insulin-resistant and insulin-sensitive men had similar postprandial chylomicron and chylomicron remnant TG concentrations, but insulin-resistant men had higher postprandial VLDL TG concentrations (median [range]; area under the curve 485 micromol/l [123-992] vs. 287 micromol/l [162-510]; P < 0.05). At 360 min, most of the difference in VLDL TGs was accounted for by an additional contribution from splanchnic fat (means +/- SE; 331 +/- 76 micromol/l vs. 89 +/- 25 micromol/l; P < 0.01). The contribution of fatty acids from endogenous systemic NEFAs was similar across the groups, as were dietary fatty acids. There was no difference in the VLDL TG concentration or the contribution of different fatty acid sources between insulin-sensitive men and women.
In the postprandial period, the only sources of fatty acids for VLDL TG production to differ in the insulin-resistant compared with the insulin-sensitive men are those derived from splanchnic sources.
我们旨在确定不同脂肪酸来源对不同程度胰岛素抵抗的健康男性和女性餐后极低密度脂蛋白甘油三酯（TGs）的贡献差异。
对胰岛素抵抗（n = 11）和胰岛素敏感（n = 11）的男性和女性（n = 6）静脉输注[(2)H(2)]棕榈酸，以研究全身非酯化脂肪酸（NEFA）掺入极低密度脂蛋白甘油三酯的情况。参与者还食用了含有[U-(13)C]棕榈酸的混合餐，以研究膳食脂肪酸对极低密度脂蛋白甘油三酯生成的贡献。在接下来的6小时内采集血样。通过密度梯度超速离心和载脂蛋白B - 100特异性免疫亲和技术分离极低密度脂蛋白。
胰岛素抵抗和胰岛素敏感的男性餐后乳糜微粒和乳糜微粒残粒甘油三酯浓度相似，但胰岛素抵抗的男性餐后极低密度脂蛋白甘油三酯浓度更高（中位数[范围]；曲线下面积485微摩尔/升[123 - 992]对287微摩尔/升[162 - 510]；P < 0.05）。在360分钟时，极低密度脂蛋白甘油三酯的大部分差异是由内脏脂肪的额外贡献所致（均值±标准误；331±76微摩尔/升对89±25微摩尔/升；P < 0.01）。内源性全身非酯化脂肪酸的脂肪酸贡献在各组之间相似，膳食脂肪酸也是如此。胰岛素敏感的男性和女性之间，极低密度脂蛋白甘油三酯浓度或不同脂肪酸来源的贡献没有差异。
在餐后期间，与胰岛素敏感男性相比，胰岛素抵抗男性中极低密度脂蛋白甘油三酯生成的脂肪酸唯一不同来源是来自内脏的脂肪酸。
