{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T22:26:42Z","timestamp":1791239202808,"version":"4.1.0"},"reference-count":27,"publisher":"American Diabetes Association","issue":"6","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2005,6,1]]},"abstract":"<jats:p>The nuclear receptor peroxisome proliferator\u2013activated receptor-\u03b3 (PPAR\u03b3) is critically required for adipogenesis. PPAR\u03b3 exists as two isoforms, \u03b31 and \u03b32. PPAR\u03b32 is the more potent adipogenic isoform in vitro and is normally restricted to adipose tissues, where it is regulated more by nutritional state than PPAR\u03b31. To elucidate the relevance of the PPAR\u03b32 in vivo, we generated a mouse model in which the PPAR\u03b32 isoform was specifically disrupted. Despite similar weight, body composition, food intake, energy expenditure, and adipose tissue morphology, male mice lacking the \u03b32 isoform were more insulin resistant than wild-type animals when fed a regular diet. These results indicate that insulin resistance associated with ablation of PPAR\u03b32 is not the result of lipodystrophy and suggests a specific role for PPAR\u03b32 in maintaining insulin sensitivity independently of its effects on adipogenesis. Furthermore, PPAR\u03b32 knockout mice fed a high-fat diet did not become more insulin resistant than those on a normal diet, despite a marked increase in their mean adipocyte cell size. These findings suggest that PPAR\u03b32 is required for the maintenance of normal insulin sensitivity in mice but also raises the intriguing notion that PPAR\u03b32 may be necessary for the adverse effects of a high-fat diet on carbohydrate metabolism.<\/jats:p>","DOI":"10.2337\/diabetes.54.6.1706","type":"journal-article","created":{"date-parts":[[2007,3,6]],"date-time":"2007-03-06T19:04:22Z","timestamp":1173207862000},"page":"1706-1716","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":152,"title":["The Link Between Nutritional Status and Insulin Sensitivity Is Dependent on the Adipocyte-Specific Peroxisome Proliferator\u2013Activated Receptor-\u03b32 Isoform"],"prefix":"10.2337","volume":"54","author":[{"given":"Gema","family":"Medina-Gomez","sequence":"first","affiliation":[{"name":"Department of Clinical Biochemistry, Histopathology, Physiology and Oncology, University of Cambridge\/Addenbrooke\u2019s Hospital, 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