Replacing dietary glucose with fructose increases ChREBP activity and SREBP-1 protein in rat liver nucleus
Replacing dietary glucose with fructose increases ChREBP activity and SREBP-1 protein in rat liver nucleus
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DOI：
10.1016/j.bbrc.2009.09.109
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发表时间：
2009-12-11
影响因子：
3.1
通讯作者：
Nakamura, Manabu T.
中科院分区：
文献类型：
--
作者：
Koo, Hyun-Young;Miyashita, Michio;Nakamura, Manabu T.
高果糖饮食导致高甘油三酯血症和胰岛素抵抗，部分原因是肝脏中糖异生和脂肪生成基因同时被诱导。我们研究了膳食果糖独特的基因诱导模式的机制。雄性Sprague-Dawley大鼠（每组n = 6）饲喂含63% （w/w）葡萄糖或63%果糖的膳食（4 h/d）。两周后，动物在最后一餐结束时被杀死。果糖喂养大鼠的核SREBP-1比葡萄糖喂养大鼠高2.2倍。果糖组核狐：01蛋白含量升高1.7倍，但未达到显著性水平（P = 0.08）。出乎意料的是，两组之间的核ChREBP没有差异。然而，在果糖喂养的动物中，ChREBP的DNA结合率提高了3.9倍，而木醛糖-5-磷酸（一种被提议的ChREBP激活剂）的含量没有增加。综上所述，膳食果糖的基因诱导可能部分是通过同时增加细胞核中ChREBP活性、SREBP-1和fox01蛋白来介导的。(C) 2009爱思唯尔公司版权所有。
Diets high in fructose cause hypertriglyceridemia and insulin resistance in part due to simultaneous induction of gluconeogenic and lipogenic genes in liver. We investigated the mechanism underlying the unique pattern of gene induction by dietary fructose. Male Sprague-Dawley rats (n = 6 per group) were meal-fed (4 h/d) either 63% (w/w) glucose or 63% fructose diet. After two weeks, animals were killed at the end of the last meal. Nuclear SREBP-1 was 2.2 times higher in fructose-fed rats than glucose-fed rats. Nuclear Fox:01 was elevated 1.7 times in fructose group, but did not reach significance (P = 0.08). Unexpectedly, no difference was observed in nuclear ChREBP between two groups. However, ChREBP DNA binding was 3.9x higher in fructose-fed animals without an increase in xylulose-5-phospate, a proposed ChREBP activator. In conclusion, the gene induction by dietary fructose is likely to be mediated in part by simultaneously increased ChREBP activity, SREBP-1 and possibly FoxO1 protein in nucleus. (C) 2009 Elsevier Inc. All rights reserved.