The AKTion in non-canonical insulin signaling

被引：27

作者：

Cheng, Zhiyong ^{[1
]}

White, Morris F. ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Howard Hughes Med Inst, Div Endocrinol,Childrens Hosp Boston, Boston, MA 02115 USA

来源：

NATURE MEDICINE | 2012年 / 18卷 / 03期

关键词：

CREB-BINDING-PROTEIN; HEPATIC GLUCONEOGENESIS; FOXO1; RESISTANCE; PHOSPHORYLATION; METFORMIN; LIVER;

D O I：

10.1038/nm.2694

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The kinase AKT has been regarded as an obligate intermediate in the insulin signaling pathway that suppresses glucose production by inhibiting the transcription factor forkhead box O1 (FoxO1) after meals. A new study shows that, without AKT-FoxO1 signaling, insulin still contributes to postprandial responses, revealing an AKT-independent pathway for insulin action that might be exploited to treat metabolic disease (pages 388-395).

引用

页码：351 / 353

页数：3

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