期刊
MOLECULAR METABOLISM
卷 3, 期 4, 页码 394-407出版社
ELSEVIER
DOI: 10.1016/j.molmet.2014.01.014
关键词
Rictor; mTORC2; CNS insulin; POMC neurons; AgRP neurons; Energy balance; Food intake; Obesity
资金
- NIDDK NIH HHS [T35 DK007383, F31 DK083222, R01 DK085712, U24 DK059637, T32 DK007563, K08 DK064857, P30 DK020593, P30 DK058404, T32 DK007044, P60 DK020593] Funding Source: Medline
Insulin signaling in the central nervous system (CNS) regulates energy balance and peripheral glucose homeostasis. Rictor is a key regulatory/ structural subunit of the mTORC2 complex and is required for hydrophobic motif site phosphorylation of Aid at serine 473. To examine the contribution of neuronal Rictor/mTORC2 signaling to CNS regulation of energy and glucose homeostasis, we utilized Cre-LoxP technology to generate mice lacking Rictor in all neurons, or in either POMC or AgRP expressing neurons. Rictor deletion in all neurons led to increased fat mass and adiposity, glucose intolerance and behavioral leptin resistance. Disrupting Rictor in POMC neurons also caused obesity and hyperphagia, fasting hyperglycemia and pronounced glucose intolerance. AgRP neuron specific deletion did not impact energy balance but led to mild glucose intolerance. Collectively, we show that Rictor/mTORC2 signaling, especially in POMC-expressing neurons, is important for central regulation of energy and glucose homeostasis. Published by Elsevier GmbH. Open access under CC BY-NC-ND license.
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