{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T12:23:38Z","timestamp":1790511818735,"version":"4.1.0"},"reference-count":59,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2006,9,13]],"date-time":"2006-09-13T00:00:00Z","timestamp":1158105600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2006,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Diabetes type I is associated with bone loss and increased bone adiposity. Osteoblasts and adipocytes are both derived from mesenchymal stem cells located in the bone marrow, therefore we hypothesized that if we could block adipocyte differentiation we might prevent bone loss in diabetic mice. Control and insulin\u2010deficient diabetic BALB\/c mice were chronically treated with a peroxisomal proliferator\u2010activated receptor \u03b3 (PPAR\u03b3) antagonist, bisphenol\u2010A\u2010diglycidyl ether (BADGE), to block adipocyte differentiation. Effects on bone density, adiposity, and gene expression were measured. BADGE treatment did not prevent diabetes\u2010associated hyperglycemia or weight loss, but did prevent diabetes\u2010induced hyperlipidemia and effectively blocked diabetes type I\u2010induced bone adiposity. Despite this, BADGE treatment did not prevent diabetes type I suppression of osteoblast markers (runx2 and osteocalcin) and bone loss (as determined by micro\u2010computed tomography). BADGE did not suppress osteoblast gene expression or bone mineral density in control mice, however, chronic (but not acute) BADGE treatment did suppress osteocalcin expression in osteoblasts in vitro. Taken together, our findings suggest that BADGE treatment is an effective approach to reduce serum triglyceride and free fatty acid levels as well as bone adiposity associated with type I diabetes. The inability of BADGE treatment to prevent bone loss in diabetic mice suggests that marrow adiposity is not linked to bone density status in type I diabetes, but we cannot exclude the possibility of additional BADGE effects on osteoblasts or other bone cells, which could contribute to preventing the rescue of the bone phenotype. J. Cell. Physiol. 209: 967\u2013976, 2006. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.20804","type":"journal-article","created":{"date-parts":[[2006,9,13]],"date-time":"2006-09-13T20:25:01Z","timestamp":1158179101000},"page":"967-976","source":"Crossref","is-referenced-by-count":105,"title":["Inhibition of PPAR\u03b3 prevents type I diabetic bone marrow adiposity but not bone loss"],"prefix":"10.1002","volume":"209","author":[{"given":"Sergiu","family":"Botolin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura R.","family":"McCabe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,9,13]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.2002.17.4.668"},{"key":"e_1_2_6_3_1","first-page":"151","article-title":"Plasticity and regulation of human bone marrow stromal osteoprogenitor cells: 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