Phosphatidyl inositol 3-kinase signaling in hypothalamic proopiomelanocortin neurons contributes to the regulation of glucose homeostasis.

Détails

ID Serval
serval:BIB_8E43557A01D3
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Phosphatidyl inositol 3-kinase signaling in hypothalamic proopiomelanocortin neurons contributes to the regulation of glucose homeostasis.
Périodique
Endocrinology
Auteur(s)
Hill J.W., Xu Y., Preitner F., Fukuda M., Cho Y.R., Luo J., Balthasar N., Coppari R., Cantley L.C., Kahn B.B., Zhao J.J., Elmquist J.K.
ISSN
1945-7170[electronic]
Statut éditorial
Publié
Date de publication
2009
Volume
150
Numéro
11
Pages
4874-4882
Langue
anglais
Résumé
Recent studies demonstrated a role for hypothalamic insulin and leptin action in the regulation of glucose homeostasis. This regulation involves proopiomelanocortin (POMC) neurons because suppression of phosphatidyl inositol 3-kinase (PI3K) signaling in these neurons blunts the acute effects of insulin and leptin on POMC neuronal activity. In the current study, we investigated whether disruption of PI3K signaling in POMC neurons alters normal glucose homeostasis using mouse models designed to both increase and decrease PI3K-mediated signaling in these neurons. We found that deleting p85alpha alone induced resistance to diet-induced obesity. In contrast, deletion of the p110alpha catalytic subunit of PI3K led to increased weight gain and adipose tissue along with reduced energy expenditure. Independent of these effects, increased PI3K activity in POMC neurons improved insulin sensitivity, whereas decreased PI3K signaling resulted in impaired glucose regulation. These studies show that activity of the PI3K pathway in POMC neurons is involved in not only normal energy regulation but also glucose homeostasis.
Mots-clé
Increased Insulin Sensitivity, Glucocorticoid-Receptor Antagonism, Pomc-Expressing Cells, Phosphoinositide 3-Kinase, Mice Lacking, Body-Weight, Energy Homeostasis, P85-Alpha Subunit, Arcuate Nucleus, Food-Intake
Pubmed
Web of science
Open Access
Oui
Création de la notice
04/11/2009 11:00
Dernière modification de la notice
08/05/2019 21:51
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