serval:BIB_4F2384AD45B8
Intestinal PPARγ signalling is required for sympathetic nervous system activation in response to caloric restriction.
10.1038/srep36937
000388151500001
27853235
Duszka
K.
author
Picard
A.
author
Ellero-Simatos
S.
author
Chen
J.
author
Defernez
M.
author
Paramalingam
E.
author
Pigram
A.
author
Vanoaica
L.
author
Canlet
C.
author
Parini
P.
author
Narbad
A.
author
Guillou
H.
author
Thorens
B.
author
Wahli
W.
author
article
2016
Scientific Reports
2045-2322
2045-2322
journal
6
36937
Nuclear receptor PPARγ has been proven to affect metabolism in multiple tissues, and has received considerable attention for its involvement in colon cancer and inflammatory disease. However, its role in intestinal metabolism has been largely ignored. To investigate this potential aspect of PPARγ function, we submitted intestinal epithelium-specific PPARγ knockout mice (iePPARγKO) to a two-week period of 25% caloric restriction (CR), following which iePPARγKO mice retained more fat than their wild type littermates. In attempting to explain this discrepancy, we analysed the liver, skeletal muscle, intestinal lipid trafficking, and the microbiome, none of which appeared to contribute to the adiposity phenotype. Interestingly, under conditions of CR, iePPARγKO mice failed to activate their sympathetic nervous system (SNS) and increase CR-specific locomotor activity. These KO mice also manifested a defective control of their body temperature, which was overly reduced. Furthermore, the white adipose tissue of iePPARγKO CR mice showed lower levels of both hormone-sensitive lipase, and its phosphorylated form. This would result from impaired SNS signalling and possibly cause reduced lipolysis. We conclude that intestinal epithelium PPARγ plays an essential role in increasing SNS activity under CR conditions, thereby contributing to energy mobilization during metabolically stressful episodes.
eng
60_published
true
peer-reviewed
University of Lausanne
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