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| Research article summary (published 30 Mar 2008): |
The ubiquitous environmental pollutant perfluorooctanoicacid inhibits feeding behavior via peroxisome proliferator-activated receptor-alpha.
Full Abstract
Perfluorinated compounds (PFCs) have been employed as surface treatment agents in a variety of products. Perfluorooctanoic acid (PFOA), a PFC that is found globally in the environment and in human tissues, has been increasing significantly in serum levels over the past 50 years. Here, we demonstrated that PFOA inhibits feeding behavior as potently as the endogenous peroxisome proliferator-activated receptor (PPAR)-alpha ligand, oleoylethanolamide (OEA), via the activation of PPAR-alpha, the vagal nerve and hypothalamic neuropeptides. Peripherally administered PFOA decreased food intake as potently as OEA. PFOA decreased gastric emptying and increased the expression level of the gene encoding urocortin 1 in the hypothalamus and the immunoreaction for urocortin 1 in the paraventricular nucleus. Vagotomy attenuated the inhibitory effects of PFOA on feeding. The inhibition of food intake and body-weight gain by PFOA was completely mitigated in PPAR-alpha-/-mice. Our studies demonstrated that the ubiquitous environmental pollutant PFOA works as an imitator of OEA mimicking its action in the feeding regulatory system, providing a new mode of action as represented by environmental 'anorexigens'.
Author information
Author/s: Asakawa, Akihiro (A); Toyoshima, Megumi (M); Harada, Kouji H (KH); Fujimiya, Mineko (M); Inoue, Kayoko (K); Koizumi, Akio (A);
Affiliation: Department of Health and Environmental Sciences, Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: International journal of molecular medicine (Int J Mol Med), published in Greece. (Language: eng)
Reference: 2008-Apr; vol 21 (issue 4) : pp 439-45
Dates: Created 2008/03/24; Completed 2008/06/05;
PMID: 18360689, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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