{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T11:09:49Z","timestamp":1790766589482,"version":"4.1.0"},"reference-count":41,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2014,7,8]],"date-time":"2014-07-08T00:00:00Z","timestamp":1404777600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01\u2010DK082659"],"award-info":[{"award-number":["R01\u2010DK082659"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007878","name":"Diabetes Research Center","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007878","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["P30\u2010DK036836"],"award-info":[{"award-number":["P30\u2010DK036836"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2014,10]]},"abstract":"<jats:p>\n                    Mitochondrial dysfunction in adipose tissue occurs in obesity, type 2 diabetes, and some forms of lipodystrophy, but whether this dysfunction contributes to or is the result of these disorders is unknown. To investigate the physiological consequences of severe mitochondrial impairment in adipose tissue, we generated mice deficient in mitochondrial transcription factor A (TFAM) in adipocytes by using mice carrying adiponectin\u2010Cre and TFAM floxed alleles. These adiponectin TFAM\u2010knockout (adipo\u2010TFAM\u2010KO) mice had a 75\u201381% reduction in TFAM in the subcutaneous and intra\u2010abdominal white adipose tissue (WAT) and interscapular brown adipose tissue (BAT), causing decreased expression and enzymatic activity of proteins in complexes I, III, and IV of the electron transport chain (ETC). This mitochondrial dysfunction led to adipocyte death and inflammation in WAT and a whitening of BAT. As a result, adipo\u2010TFAM\u2010KO mice were resistant to weight gain, but exhibited insulin resistance on both normal chow and high\u2010fat diets. These lipodystrophic mice also developed hypertension, cardiac hypertrophy, and cardiac dysfunction. Thus, isolated mitochondrial dysfunction in adipose tissue can lead a syndrome of lipodystrophy with metabolic syndrome and cardiovascular complications.\u2014Vernochet, C., Damilano, F., Mourier, A., Bezy, O., Mori, M. A., Smyth, G., Rosenzweig, A., Larsson, N.\u2010G., Kahn, C. R. Adipose tissue mitochondrial dysfunction triggers a lipodystrophic syndrome with insulin resistance, hepatosteatosis, and cardiovascular complications. FASEB J. 28, 4408\u20134419 (2014).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.14-253971","type":"journal-article","created":{"date-parts":[[2014,7,8]],"date-time":"2014-07-08T23:26:46Z","timestamp":1404862006000},"page":"4408-4419","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":159,"title":["Adipose tissue mitochondrial dysfunction triggers a lipodystrophic syndrome with insulin resistance, hepatosteatosis, and cardiovascular complications"],"prefix":"10.1096","volume":"28","author":[{"given":"Cecile","family":"Vernochet","sequence":"first","affiliation":[{"name":"Section on Integrative Physiology and Metabolism Joslin Diabetes Center Boston Massachusetts USA"},{"name":"Department of Medicine Harvard Medical School Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Federico","family":"Damilano","sequence":"additional","affiliation":[{"name":"Department of Medicine Harvard Medical School Boston Massachusetts USA"},{"name":"Cardiovascular Division Department of Medicine Beth Israel Deaconess Medical Center Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arnaud","family":"Mourier","sequence":"additional","affiliation":[{"name":"Department of Mitochondrial Biology Max Planck Institute for Biology of Ageing Cologne Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivier","family":"Bezy","sequence":"additional","affiliation":[{"name":"Section on Integrative Physiology and Metabolism Joslin Diabetes Center Boston Massachusetts USA"},{"name":"Department of Medicine Harvard Medical School Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcelo A.","family":"Mori","sequence":"additional","affiliation":[{"name":"Section on Integrative Physiology and Metabolism Joslin Diabetes Center Boston Massachusetts USA"},{"name":"Department of Medicine Harvard Medical School Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Graham","family":"Smyth","sequence":"additional","affiliation":[{"name":"Section on Integrative Physiology and Metabolism Joslin Diabetes Center Boston Massachusetts USA"},{"name":"Department of Medicine Harvard Medical School Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anthony","family":"Rosenzweig","sequence":"additional","affiliation":[{"name":"Department of Medicine Harvard Medical School Boston Massachusetts USA"},{"name":"Cardiovascular Division Department of Medicine Beth Israel Deaconess Medical Center Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nils\u2010G\u00f6ran","family":"Larsson","sequence":"additional","affiliation":[{"name":"Department of Mitochondrial Biology Max Planck Institute for Biology of Ageing Cologne Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. 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