PI3K p110β subunit in leptin receptor expressing cells is required for the acute hypophagia induced by endotoxemia
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- 作者：Beatriz C. Borges1 ; 2 ; beatrizd@med.umich.edu" class="auth_mail" title="E-mail the corresponding author ; borgesbc@gmail.com" class="auth_mail" title="E-mail the corresponding author ; David Garcia-Galiano1 ; dgarciag@med.umich.edu" class="auth_mail" title="E-mail the corresponding author ; Rodrigo Rorato2 ; rcrorato@rfi.fmrp.usp.br" class="auth_mail" title="E-mail the corresponding author ; Lucila L.K. Elias2 ; llelias@fmrp.usp.br" class="auth_mail" title="E-mail the corresponding author ; Carol F. Elias1 ; 3 ; cfelias@med.umich.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：LPS ; Metabolism ; Leptin ; Hypothalamus ; Inflammation
- 刊名：Molecular Metabolism
- 出版年：2016
- 出版时间：June 2016
- 年：2016
- 卷：5
- 期：6
- 页码：379-391
- 全文大小：2753 K
文摘
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Bacterial lipopolyssacharide (LPS) stimulates PI3K pathway in hypothalamic LepR expressing cells.
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LPS-induced hypophagia is prevented by central PI3K inhibition.
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PI3K p110α subunit in LepR cells is not required for LPS-induced hypophagia.
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PI3K p110α and p110β double deletion in LepR cells prevents LPS-induced hypophagia.