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Publication
Rictor/mTORC2 facilitates central regulation of energy and glucose homeostasis.
Authors Kocalis HE, Hagan SL, George L, Turney MK, Siuta MA, Laryea GN, Morris LC,
Muglia LJ, Printz RL, Stanwood GD, Niswender KD
Submitted By Submitted Externally on 10/26/2016
Status Published
Journal Molecular metabolism
Year 2014
Date Published
Volume : Pages 3 : 394 - 407
PubMed Reference 24944899
Abstract 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 Akt 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.




Strains
StrainDevelopment StatusCreation MethodOptions
B6.129S4-Tg(Pomc1-cre)1GsbPhenotyping completenot applicable
View
B6.Cg-Rictortm1.1Mgn Tg(Nes-cre)1KlnPhenotyping completeknockout
View
B6.Cg-Rictortm1.1Mgn/+ Tg(Nes-cre)1KlnPhenotyping completeknockout
View
B6.Cg-Tg(Nes-cre)1Kln/JPhenotyping completetransgenic
View


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