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Adipocyte size in Wy-14,643\u2013treated KKAy mice was much smaller than that of vehicle- or rosiglitazone-treated mice, suggesting that activation of PPAR\u03b1 prevents adipocyte hypertrophy. Moreover, Wy-14,643 treatment reduced inflammation and the expression of macrophage-specific genes in white adipose tissue (WAT). Importantly, Wy-14,643 treatment upregulated expression of the adiponectin receptor (AdipoR)-1 and AdipoR2 in WAT, which was decreased in WAT of KKAy mice compared with that in nondiabetic control mice. Furthermore, Wy-14,643 directly increased expression of AdipoRs and decreased monocyte chemoattractant protein-1 expression in adipocytes and macrophages. Rosiglitazone increased serum adiponectin concentrations and the ratio of high molecular weight multimers of adiponectin to total adiponectin. A combination of rosiglitazone and Wy-14,643 increased both serum adiponectin concentrations and AdipoR expression in WAT. These data suggest that PPAR\u03b1 activation prevents inflammation in WAT and that dual activation of PPAR\u03b1 and -\u03b3 enhances the action of adiponectin by increasing both adiponectin and AdipoRs, which can result in the amelioration of obesity-induced insulin resistance.<\/jats:p>","DOI":"10.2337\/diabetes.54.12.3358","type":"journal-article","created":{"date-parts":[[2007,3,6]],"date-time":"2007-03-06T19:04:22Z","timestamp":1173207862000},"page":"3358-3370","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":371,"title":["Peroxisome Proliferator\u2013Activated Receptor (PPAR)\u03b1 Activation Increases Adiponectin Receptors and Reduces Obesity-Related Inflammation in Adipose Tissue"],"prefix":"10.2337","volume":"54","author":[{"given":"Atsushi","family":"Tsuchida","sequence":"first","affiliation":[{"name":"Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshimasa","family":"Yamauchi","sequence":"additional","affiliation":[{"name":"Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Tokyo, Japan"},{"name":"Core Research for Evolutional Science and Technology of Japan Science and Technology Agency, Kawaguchi, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sato","family":"Takekawa","sequence":"additional","affiliation":[{"name":"Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yusuke","family":"Hada","sequence":"additional","affiliation":[{"name":"Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yusuke","family":"Ito","sequence":"additional","affiliation":[{"name":"Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshiyuki","family":"Maki","sequence":"additional","affiliation":[{"name":"Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takashi","family":"Kadowaki","sequence":"additional","affiliation":[{"name":"Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Tokyo, Japan"},{"name":"Core Research for Evolutional Science and Technology of Japan Science and Technology Agency, Kawaguchi, Japan"},{"name":"National Institute of Health and Nutrition, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","reference":[{"key":"2022031209125379800_R1","doi-asserted-by":"crossref","unstructured":"Kersten S, Desvergne B, Wahli W: Roles of PPARs in health and disease. 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