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Toxicol Sci. 2015 Aug;146(2):334-43. doi: 10.1093/toxsci/kfv098. Epub 2015 May 21.

The Environmental Pollutants Perfluorooctane Sulfonate and Perfluorooctanoic Acid Upregulate Uncoupling Protein 1 (UCP1) in Brown-Fat Mitochondria Through a UCP1-Dependent Reduction in Food Intake.

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*Department of Molecular Biosciences, The Wenner-Gren Institute;
The Arrhenius Laboratories F3, Department of Biochemistry and Biophysics, Stockholm University, SE-106 91 Stockholm, Sweden; and.
Medical Department, 3 M Center, St. Paul, Minnesota 55144.
*Department of Molecular Biosciences, The Wenner-Gren Institute;


The environmental pollutants perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) cause a dramatic reduction in the size of the major adipose tissue depots and a general body weight decrease when they are added to the food of mice. We demonstrate here that this is mainly due to a reduction in food intake; this reduction was not due to food aversion. Remarkably and unexpectedly, a large part of the effect of PFOA/PFOS on food intake was dependent on the presence of the uncoupling protein 1 (UCP1) in the mice. Correspondingly, PFOA/PFOS treatment induced recruitment of brown adipose tissue mitochondria: increased oxidative capacity and increased UCP1-mediated oxygen consumption (thermogenesis). In mice pair-fed to the food intake during PFOA/PFOS treatment in wildtype mice, brown-fat mitochondrial recruitment was also induced. We conclude that we have uncovered the existence of a regulatory component of food intake that is dependent upon brown adipose tissue thermogenic activity. The possible environmental consequences of this novel PFOA/PFOS effect (a possible decreased fitness) are noted, as well as the perspectives of this finding on the general understanding of control of food intake control and its possible extension to combatting obesity.


adipose tissue; body temperature; fatty acid oxidation; food restriction; thermogenesis

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