NATURE:微生物代谢膳食果糖,促进肝脏脂肪生成

2020-03-22 MedSci原创 MedSci原创

饮食中的果糖通过肠道微生物转化为醋酸盐,从而独立于ACLY,提供脂肪生成所需的乙酰辅酶a。

近几十年来,由于在饮料和加工食品中使用蔗糖和高果糖玉米糖浆,人群果糖的摄入量显著增加,这导致了肥胖率和非酒精性脂肪肝发病率的增加。

已有的研究显示,果糖的摄入会引发肝脏脂肪的从头合成,在这个过程中,乙酰辅酶a作为碳前体会被转化为脂肪酸。ATP柠檬酸裂解酶(ACLY)分解胞质柠檬酸生成乙酰辅酶a,并在消耗碳水化合物后上调。临床试验目前正在将抑制ACLY作为治疗代谢性疾病的一种方法。

然而,至今为止,饮食果糖如何转变为肝乙酰辅酶a和脂质仍然未知。

最近,通过体内同位素追踪,研究人员发现Acly在小鼠肝脏特异性的缺失并不能抑制果糖诱导的脂肪生成。饮食中的果糖通过肠道微生物转化为醋酸盐,从而独立于ACLY,提供脂肪生成所需的乙酰辅酶a。

微生物群的减少或肝ACSS2的沉默(ACSS2帮助乙酸产生乙酰辅酶a),可以有效地抑制大剂量果糖转化为肝乙酰辅酶a和脂肪酸。当果糖逐渐被摄取,以促进其在小肠中的吸收时,肝细胞中的柠檬酸裂解和微生物来源的醋酸盐都有助于脂肪生成。

相比之下,脂质转录程序在对果糖的反应中被激活,其方式与乙酰辅酶a的代谢无关。

这些数据揭示了调节肝脏脂肪生成的双重机制,其中肝细胞内的果糖分解为促进脂肪生成基因的表达提供了一个信号,而微生物乙酸盐的生成为乙酰辅酶a的脂肪生成库提供了原料。

 

原始出处:

Steven Zhao et al. Dietary fructose feeds hepatic lipogenesis via microbiota-derived acetate. NATURE, 2020; 

 

 

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    2020-11-30 liye789132251
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    2020-03-24 zhaojie88
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