High-fat feeding promotes obesity via insulin receptor/PI3K-dependent inhibition of SF-1 VMH neurons View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2011-07

AUTHORS

Tim Klöckener, Simon Hess, Bengt F Belgardt, Lars Paeger, Linda A W Verhagen, Andreas Husch, Jong-Woo Sohn, Brigitte Hampel, Harveen Dhillon, Jeffrey M Zigman, Bradford B Lowell, Kevin W Williams, Joel K Elmquist, Tamas L Horvath, Peter Kloppenburg, Jens C Brüning

ABSTRACT

Steroidogenic factor 1 (SF-1)-expressing neurons of the ventromedial hypothalamus (VMH) control energy homeostasis, but the role of insulin action in these cells remains undefined. We show that insulin activates phosphatidylinositol-3-OH kinase (PI3K) signaling in SF-1 neurons and reduces firing frequency in these cells through activation of K(ATP) channels. These effects were abrogated in mice with insulin receptor deficiency restricted to SF-1 neurons (SF-1(ΔIR) mice). Whereas body weight and glucose homeostasis remained the same in SF-1(ΔIR) mice as in controls under a normal chow diet, they were protected from diet-induced leptin resistance, weight gain, adiposity and impaired glucose tolerance. High-fat feeding activated PI3K signaling in SF-1 neurons of control mice, and this response was attenuated in the VMH of SF-1(ΔIR) mice. Mimicking diet-induced overactivation of PI3K signaling by disruption of the phosphatidylinositol-3,4,5-trisphosphate phosphatase PTEN led to increased body weight and hyperphagia under a normal chow diet. Collectively, our experiments reveal that high-fat diet-induced, insulin-dependent PI3K activation in VMH neurons contributes to obesity development. More... »

PAGES

911

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nn.2847

DOI

http://dx.doi.org/10.1038/nn.2847

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1007053573

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21642975


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