Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 355510
Title Peroxisome Proliferator-Activated Receptor : alpha Protects against Obesity-Induced Hepatic Inflammation
Author(s) Stienstra, R.; Mandard, S.J.; Patsouris, D.A.; Maass, C.; Kersten, A.H.; Müller, M.R.
Source Endocrinology 148 (2007)6. - ISSN 0013-7227 - p. 2753 - 2763.
DOI https://doi.org/10.1210/en.2007-0014
Department(s) Nutrition, Metabolism and Genomics
VLAG
Publication type Refereed Article in a scientific journal
Publication year 2007
Keyword(s) nf-kappa-b - ppar-alpha - insulin-resistance - adipose-tissue - gene-expression - ikk-beta - in-vivo - liver - mice - steatohepatitis
Abstract Recently it has become evident that obesity is associated with low-grade chronic inflammation. The transcription factor peroxisome proliferator-activated receptor (PPAR) has been shown to have a strong antiinflammatory action in liver. However, the role of PPAR in obesity-induced inflammation is much less clear. Therefore, the aim of our study was to determine whether PPAR plays a role in obesity-induced hepatic inflammation. To induce obesity, wild-type sv129 and PPAR¿/¿ mice were exposed to a chronic high-fat diet (HFD), using a low-fat diet (LFD) as control. In wild-type mice, HFD significantly increased the hepatic and adipose expression of numerous genes involved in inflammation. Importantly, this effect was amplified in PPAR¿/¿ mice, suggesting an antiinflammatory role of PPAR in liver and adipose tissue. Further analysis identified specific chemokines and macrophage markers, including monocyte chemotactic protein 1 and F4/80+, that were elevated in liver and adipose tissue of PPAR¿/¿ mice, indicating increased inflammatory cell recruitment in the knockout animals. When all groups of mice were analyzed together, a significant correlation between hepatic triglycerides and expression of inflammatory markers was observed. Many inflammatory genes that were up-regulated in PPAR¿/¿ livers by HFD were down-regulated by treatment with the PPAR ligand Wy-14643 under normal nonsteatotic conditions, either in vivo or in vitro, suggesting an antiinflammatory effect of PPAR that is independent of reduction in liver triglycerides. In conclusion, our results suggest that PPAR protects against obesity-induced chronic inflammation in liver by reducing hepatic steatosis, by direct down-regulation of inflammatory genes, and by attenuating inflammation in adipose tissue.
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