mmpc-logo mmpc-logo
twitter-logo    bluesky-logo
| Create Account | login
Publication
Adipose tissue mTORC2 regulates ChREBP-driven de novo lipogenesis and hepatic
glucose metabolism.
Authors Tang Y, Wallace M, Sanchez-Gurmaches J, Hsiao WY, Li H, Lee PL, Vernia S,
Metallo CM, Guertin DA
Submitted By Submitted Externally on 9/22/2017
Status Published
Journal Nature communications
Year 2016
Date Published 4/21/2016
Volume : Pages 7 : 11365
PubMed Reference 27098609
Abstract Adipose tissue de novo lipogenesis (DNL) positively influences insulin
sensitivity, is reduced in obesity, and predicts insulin resistance. Therefore,
elucidating mechanisms controlling adipose tissue DNL could lead to therapies
for type 2 diabetes. Here, we report that mechanistic target of rapamycin
complex 2 (mTORC2) functions in white adipose tissue (WAT) to control expression
of the lipogenic transcription factor ChREBPß. Conditionally deleting the
essential mTORC2 subunit Rictor in mature adipocytes decreases ChREBPß
expression, which reduces DNL in WAT, and impairs hepatic insulin sensitivity.
Mechanistically, Rictor/mTORC2 promotes ChREBPß expression in part by
controlling glucose uptake, but without impairing pan-AKT signalling. High-fat
diet also rapidly decreases adipose tissue ChREBPß expression and insulin
sensitivity in wild-type mice, and does not further exacerbate insulin
resistance in adipose tissue Rictor knockout mice, implicating adipose tissue
DNL as an early target in diet-induced insulin resistance. These data suggest
mTORC2 functions in WAT as part of an extra-hepatic nutrient-sensing mechanism
to control glucose homeostasis.








Genes
SymbolDescription
Adipoqadiponectin, C1Q and collagen domain containing
RictorRictor RPTOR independent companion of MTOR, complex 2

Menu

Home
Contact
About MMPC
Animal Husbandry
Tests Data
Search Data
Analysis
Clients
MMPC Centers

Newsletter

Interested in receiving MMPC News?
twitter-logo Mouse Phenotyping
@NationalMMPC



2017 National MMPC. All Rights Reserved.