Chong Mary F-F, Hodson Leanne, Bickerton Alex S, Roberts Rachel, Neville Matt, Karpe Fredrik, Frayn Keith N, Fielding Barbara A
Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom.
Am J Clin Nutr. 2008 Apr;87(4):817-23. doi: 10.1093/ajcn/87.4.817.
High-carbohydrate (HC) diets increase de novo lipogenesis (DNL), but effects on stearoyl-CoA desaturase (SCD) are not so well studied.
The objective was to investigate DNL and SCD in liver and adipose tissue by using fatty acid ratios after short-term dietary intervention.
Eight subjects consumed isoenergetic 3-d HC (10% fat; 75% carbohydrates) or higher fat (HF; 40% fat; 45% carbohydrates) diets (sugar to starch ratio: 60:40 for both) in a crossover study. Blood was taken from an artery and a vein draining subcutaneous adipose tissue. DNL and SCD activity were investigated by using the ratios of 16:0 to 18:2n-6 and of 16:1n-7 to 16:0, respectively. A test meal, including [U-(13)C]palmitate was given to trace dietary fatty acid incorporation into VLDL-triacylglycerol (TG). The conversion of intravenously infused [(2)H(2)]palmitic acid to [(2)H(2)]palmitoleic acid in VLDL-TG was quantified as a specific marker of hepatic SCD activity.
The VLDL-TG 16:0/18:2n-6 ratio, which reflects hepatic DNL, was greater after the HC diet than after the HF diet (P = 0.02). With the HC diet, increased plasma TG concentrations correlated with 16:0/18:2n-6 ratios (r = 0.76, P = 0.028). Plasma VLDL-TG and adipose venous nonesterified fatty acid (NEFA) 16:1n-7/16:0 ratios were higher after the HC diet (fasting: P = 0.01 and P = 0.05, respectively; postprandial: P = 0.03 and P = 0.05, respectively). Changes in fasting VLDL-TG 16:0/18:2n-6 and 16:1n-7/16:0 ratios were associated (P = 0.06). The contribution of total fatty acids from splanchnic sources (including DNL) was higher after the HC diet (P = 0.02). Expression of lipogenic genes in subcutaneous adipose tissue was not significantly affected by diet.
Parallel activation of DNL and SCD was found after a short period of HC feeding.
高碳水化合物（HC）饮食会增加从头脂肪生成（DNL），但对硬脂酰辅酶A去饱和酶（SCD）的影响尚未得到充分研究。
通过短期饮食干预后使用脂肪酸比例来研究肝脏和脂肪组织中的DNL和SCD。
在一项交叉研究中，8名受试者分别食用等能量的3天HC饮食（10%脂肪；75%碳水化合物）或高脂肪（HF；40%脂肪；45%碳水化合物）饮食（两种饮食的糖与淀粉比例均为60:40）。从动脉和引流皮下脂肪组织的静脉采集血液。分别使用16:0与18:2n-6以及16:1n-7与16:0的比例来研究DNL和SCD活性。给予一顿测试餐，其中包括[U-(13)C]棕榈酸，以追踪膳食脂肪酸掺入极低密度脂蛋白-三酰甘油（TG）的情况。将静脉输注的[(2)H(2)]棕榈酸在极低密度脂蛋白-TG中转化为[(2)H(2)]棕榈油酸的量定量为肝脏SCD活性的特异性标志物。
反映肝脏DNL的极低密度脂蛋白-TG的16:0/18:2n-6比例，在HC饮食后高于HF饮食后（P = 0.02）。采用HC饮食时，血浆TG浓度升高与16:0/18:2n-6比例相关（r = 0.76，P = 0.028）。HC饮食后，血浆极低密度脂蛋白-TG和脂肪静脉非酯化脂肪酸（NEFA）的16:1n-7/16:0比例更高（空腹时：分别为P = 0.01和P = 0.05；餐后：分别为P = 0.03和P = 0.05）。空腹极低密度脂蛋白-TG的16:0/18:2n-6和16:1n-7/16:0比例的变化具有相关性（P = 0.06）。HC饮食后，来自内脏来源的总脂肪酸（包括DNL）的贡献更高（P = 0.02）。皮下脂肪组织中脂肪生成基因的表达未受到饮食的显著影响。
短期给予HC饮食后发现DNL和SCD同时被激活。
