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Title: Intestinal PPARγ signalling is required for sympathetic nervous system activation in response to caloric restriction
Authors: Duszka, Kalina
Picard, Alexandre
Ellero-Simatos, Sandrine
Chen, Jiapeng
Defernez, Marianne
Paramalingam, Eeswari
Pigram, Anna
Vanoaica, Liviu
Canlet, Cécile
Parini, Paolo
Narbad, Arjan
Guillou, Hervé
Thorens, Bernard
Wahli, Walter
Keywords: Gene expression
Issue Date: 2016
Source: Duszka, K., Picard, A., Ellero-Simatos, S., Chen, J., Defernez, M., Paramalingam, E., et al. (2016). Intestinal PPARγ signalling is required for sympathetic nervous system activation in response to caloric restriction. Scientific Reports, 6, 36937-.
Series/Report no.: Scientific Reports
Abstract: 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.
ISSN: 2045-2322
DOI: 10.1038/srep36937
Rights: © 2016 The Authors. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit
Fulltext Permission: open
Fulltext Availability: With Fulltext
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