{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T22:19:32Z","timestamp":1783549172423,"version":"3.55.0"},"reference-count":48,"publisher":"American Diabetes Association","issue":"10","license":[{"start":{"date-parts":[[2017,9,20]],"date-time":"2017-09-20T00:00:00Z","timestamp":1505865600000},"content-version":"vor","delay-in-days":75,"URL":"http:\/\/www.diabetesjournals.org\/content\/license"}],"funder":[{"DOI":"10.13039\/100004336","name":"Novartis","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100004336","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Bo & Kerstin Hjelt Foundation"},{"name":"Sir Jules Thorn Charitable Overseas Trust Reg."}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2017,10,1]]},"abstract":"<jats:p>Peroxisome proliferator\u2013activated receptor \u03b3 (PPAR\u03b3) is a master regulator of energy metabolism. In bone, it is known to regulate osteoblast differentiation and osteoclast activity. Whether PPAR\u03b3 expression in bone cells, particularly osteocytes, regulates energy metabolism remains unknown. Here, we show that mature osteoblast\/osteocyte-specific ablation of PPAR\u03b3 in mice (Ocy-PPAR\u03b3\u2212\/\u2212) alters body composition with age, namely, to produce less fat and more lean mass, and enhances insulin sensitivity and energy expenditure compared with wild-type mice. In addition, Ocy-PPAR\u03b3\u2212\/\u2212 mice exhibit more bone density, structure, and strength by uncoupling bone formation from resorption. When challenged with a high-fat diet, Ocy-PPAR\u03b3\u2212\/\u2212 mice retain glycemic control, with increased browning of the adipose tissue, decreased gluconeogenesis, and less hepatic steatosis. Moreover, these metabolic effects, particularly an increase in fatty acid oxidation, cannot be explained by decarboxylated osteocalcin changes, suggesting existence of other osteokines that are under the control of PPAR\u03b3. We further identify bone morphogenetic protein 7 as one of them. Hence, osteocytes coregulate bone and glucose homeostasis through a PPAR\u03b3 regulatory pathway, and its inhibition could be clinically relevant for the prevention of glucose metabolic disorders.<\/jats:p>","DOI":"10.2337\/db17-0116","type":"journal-article","created":{"date-parts":[[2017,7,7]],"date-time":"2017-07-07T20:25:36Z","timestamp":1499459136000},"page":"2541-2554","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":43,"title":["Bone Regulates Browning and Energy Metabolism Through Mature Osteoblast\/Osteocyte PPAR\u03b3 Expression"],"prefix":"10.2337","volume":"66","author":[{"given":"Julia","family":"Brun","sequence":"first","affiliation":[{"name":"Division of Bone Diseases, Department of Internal Medicine Specialties, Faculty of Medicine, Geneva University Hospital, Geneva, 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