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Inhibition of Notch signaling ameliorates insulin resistance in a FoxO1-dependent manner.

Abstract：

:Transcription factor FoxO1 promotes hepatic glucose production. Genetic inhibition of FoxO1 function prevents diabetes in experimental animal models, providing impetus to identify pharmacological approaches to modulate this function. Altered Notch signaling is evident in tumorigenesis, and Notch antagonists are in clinical testing for application in cancer. Here we report that FoxO1 and Notch coordinately regulate hepatic glucose metabolism. Combined haploinsufficiency of FoxO1 and Notch1 markedly raises insulin sensitivity in diet-induced insulin resistance, as does liver-specific knockout of the Notch transcriptional effector Rbp-Jκ. Conversely, Notch1 gain-of-function promotes insulin resistance in a FoxO1-dependent manner and induces glucose-6-phosphatase expression. Pharmacological blockade of Notch signaling with γ-secretase inhibitors raises insulin sensitivity after in vivo administration in lean mice and in obese, insulin-resistant mice. The data identify a heretofore unknown metabolic function of Notch and suggest that Notch inhibition is beneficial in diabetes treatment, in part by helping to offset excessive FoxO1-driven hepatic glucose production.

journal_name

Nat Med

journal_title

Nature medicine

authors

Pajvani UB,Shawber CJ,Samuel VT,Birkenfeld AL,Shulman GI,Kitajewski J,Accili D

doi

10.1038/nm.2378

subject

Has Abstract

pub_date

2011-07-31 00:00:00

pages

961-7

issue

8

eissn

1078-8956

issn

1546-170X

pii

nm.2378

journal_volume

17

pub_type

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