Diraison Frédérique, Yankah Vivienne, Letexier Dominique, Dusserre Eric, Jones Peter, Beylot Michel
INSERM U 499 and GENALYS, Faculté RTH Laennec, 69008, Lyon, France.
J Lipid Res. 2003 Apr;44(4):846-53. doi: 10.1194/jlr.M200461-JLR200. Epub 2003 Feb 1.
We assessed the contributions of human liver and adipose tissue de novo lipogenesis (DNL) to triacylglycerol (TAG) synthesis. Volunteers were fed a high-energy, high-carbohydrate diet (HC, n = 5) or a normocaloric diet (NC, n = 10). NC subjects remained in the fasting state (Study 1, n = 5) or received oral glucose (Study 2, n = 5) throughout the test (12 h). HC subjects remained in the fasting state (Study 3). They ingested deuterated water and [U-13C]acetate to trace lipogenesis. Adipose tissue fatty-acid (FA) synthase (FAS), acetyl-CoA carboxylase 1 (ACC1), and SREBP-1c mRNA were measured. Plasma TAG-FA was labeled by 13C and deuterium showing active liver lipogenesis, which was stimulated (P < 0.05) by oral glucose and HC diet. Adipose tissue TAG had no detectable 13C enrichment in any test, showing no significant incorporation of TAG-FA provided by liver lipogenesis, but were labeled by deuterium in all tests, showing active DNL in situ; however, rough quantitative estimates showed that adipose DNL was minimal (<1 g), and poorly stimulated by oral glucose or HC diet. mRNA levels were not increased by the HC diet. Adipose DNL is active in humans, but contributes little to TAG stores and is less responsive than liver DNL to stimulation by carbohydrates.
我们评估了人类肝脏和脂肪组织从头脂肪生成（DNL）对三酰甘油（TAG）合成的贡献。志愿者被给予高能量、高碳水化合物饮食（HC，n = 5）或正常热量饮食（NC，n = 10）。NC组受试者在整个测试过程（12小时）中保持禁食状态（研究1，n = 5）或口服葡萄糖（研究2，n = 5）。HC组受试者保持禁食状态（研究3）。他们摄入氘水和[U-13C]乙酸盐以追踪脂肪生成。测量了脂肪组织脂肪酸（FA）合酶（FAS）、乙酰辅酶A羧化酶1（ACC1）和SREBP-1c的mRNA水平。血浆TAG-FA被13C和氘标记，表明肝脏脂肪生成活跃，口服葡萄糖和HC饮食可刺激其增加（P < 0.05）。在任何测试中，脂肪组织TAG均未检测到13C富集，表明肝脏脂肪生成提供的TAG-FA没有显著掺入，但在所有测试中均被氘标记，表明原位DNL活跃；然而，粗略的定量估计表明，脂肪组织的DNL极少（<1克），且口服葡萄糖或HC饮食对其刺激作用较弱。HC饮食并未使mRNA水平升高。脂肪组织的DNL在人类中是活跃的，但对TAG储存的贡献很小，并且与肝脏DNL相比，对碳水化合物刺激的反应较弱。
