{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T06:45:39Z","timestamp":1791096339727,"version":"4.1.0"},"reference-count":49,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2012,3,28]],"date-time":"2012-03-28T00:00:00Z","timestamp":1332892800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The regulation of bone and fat homeostasis and its relationship to energy expenditure has recently been the focus of increased attention because of its potential relevance to osteoporosis, obesity, and diabetes. Although central effectors within the hypothalamus have been shown to contribute to the regulation of both energy balance and bone homeostasis, little is known of the underlying mechanisms, including the possible involvement of transcriptional factors within the hypothalamus. Transgenic mice overexpressing \u0394FosB, a splice variant of the AP-1 transcription factor FosB with mixed agonist-antagonistic properties, have increased energy expenditure and bone mass. Because these mice express \u0394FosB in bone, fat, and hypothalamus, we sought to determine 1) whether overexpression of \u0394FosB within the hypothalamus was sufficient to regulate energy expenditure and whether it would also regulate bone mass, and 2) whether these effects were the result of antagonism to AP-1. Our results show that stereotactic injection of an adeno-associated virus vector to restrict overexpression of \u0394FosB to the ventral hypothalamus of wild-type mice induced a profound increase in both energy expenditure and bone formation and bone mass. This effect was phenocopied, at an even stronger level, by overexpression of a dominant-negative DNJunD, a pure AP-1 antagonist. Taken together, these results suggest that downregulation of AP-1 activity in the hypothalamus profoundly increases energy expenditure and bone formation, leading to both a decrease in adipose mass and an increase in bone mass. These findings may have physiological implications because \u0394FosB is expressed and regulated in the hypothalamus. \u00a9 2012 American Society for Bone and Mineral Research.<\/jats:p>","DOI":"10.1002\/jbmr.1618","type":"journal-article","created":{"date-parts":[[2012,3,31]],"date-time":"2012-03-31T00:39:38Z","timestamp":1333154378000},"page":"1649-1658","source":"Crossref","is-referenced-by-count":17,"title":["Energy expenditure and bone formation share a common sensitivity to AP-1 transcription in the hypothalamus"],"prefix":"10.1093","volume":"27","author":[{"given":"Glenn C","family":"Rowe","sequence":"first","affiliation":[{"name":"Cardiovascular Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA."},{"name":"Department of Medicine, Harvard Medical School, Endocrine Unit, Massachusetts General Hospital, and Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vincent","family":"Vialou","sequence":"additional","affiliation":[{"name":"Fishberg Department of Neuroscience and Friedman Brain Institute, Mount Sinai School of Medicine, New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazusa","family":"Sato","sequence":"additional","affiliation":[{"name":"Department of Medicine, Harvard Medical School, Endocrine Unit, Massachusetts General Hospital, and Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroaki","family":"Saito","sequence":"additional","affiliation":[{"name":"Department of Medicine, Harvard Medical School, Endocrine Unit, Massachusetts General Hospital, and Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Min","family":"Yin","sequence":"additional","affiliation":[{"name":"Department of Medicine, Harvard Medical School, Endocrine Unit, Massachusetts General Hospital, and Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas A","family":"Green","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, The University of Texas Medical Branch, Galveston, TX, USA."},{"name":"Fishberg Department of Neuroscience and Friedman Brain Institute, Mount Sinai School of Medicine, New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sutada","family":"Lotinun","sequence":"additional","affiliation":[{"name":"Department of Medicine, Harvard Medical School, Endocrine Unit, Massachusetts General Hospital, and Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie","family":"Kveiborg","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences and Biotech Research & Innovation Center, University of Copenhagen, Copenhagen, Denmark."},{"name":"Department of Medicine, Harvard Medical School, Endocrine Unit, Massachusetts General Hospital, and Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William C","family":"Horne","sequence":"additional","affiliation":[{"name":"Department of Medicine, Harvard Medical School, Endocrine Unit, Massachusetts General Hospital, and Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric J","family":"Nestler","sequence":"additional","affiliation":[{"name":"Fishberg Department of Neuroscience and Friedman Brain Institute, Mount Sinai School of Medicine, New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roland","family":"Baron","sequence":"additional","affiliation":[{"name":"Department of Medicine, Harvard Medical School, Endocrine Unit, Massachusetts General Hospital, and Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2012,3,28]]},"reference":[{"issue":"11","key":"2024020318280778300_bib1","doi-asserted-by":"crossref","first-page":"4795","DOI":"10.1210\/jc.2010-1030","article-title":"The central regulation of bone mass, the first link between bone remodeling and energy metabolism","volume":"95","author":"Karsenty","year":"2010","journal-title":"J Clin Endocrinol 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