{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T21:26:00Z","timestamp":1791321960378,"version":"4.3.1"},"reference-count":50,"publisher":"American Diabetes Association","issue":"12","license":[{"start":{"date-parts":[[2021,8,30]],"date-time":"2021-08-30T00:00:00Z","timestamp":1630281600000},"content-version":"vor","delay-in-days":2844,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/3.0\/"}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2013,12,1]]},"abstract":"<jats:p>The beneficial metabolic actions of estrogen-based therapies are mainly mediated by estrogen receptor \u03b1 (ER\u03b1), a nuclear receptor that regulates gene transcription through two activation functions (AFs): AF-1 and AF-2. Using mouse models deleted electively for ER\u03b1AF-1 (ER\u03b1AF-1\u00b0) or ER\u03b1AF-2 (ER\u03b1AF-2\u00b0), we determined their respective roles in the actions of estrogens on body composition and glucose homeostasis in response to either a normal diet or a high-fat diet (HFD). ER\u03b1AF-2\u00b0 males and females developed accelerated weight gain, massive adiposity, severe insulin resistance, and glucose intolerance\u2014quite reminiscent of the phenotype observed in mice deleted for the entire ER\u03b1 protein (ER\u03b1\u2212\/\u2212). In striking contrast, ER\u03b1AF-1\u00b0 and wild-type (wt) mice shared a similar metabolic phenotype. Accordingly, 17\u03b2-estradiol administration regulated key metabolic genes in insulin-sensitive tissues and conferred a strong protection against HFD-induced metabolic disturbances in wt and ER\u03b1AF-1\u00b0 ovariectomized mice, whereas these actions were totally abrogated in ER\u03b1AF-2\u00b0 and ER\u03b1\u2212\/\u2212 mice. Thus, whereas both AFs have been previously shown to contribute to endometrial and breast cancer cell proliferation, the protective effect of estrogens against obesity and insulin resistance depends on ER\u03b1AF-2 but not ER\u03b1AF-1, thereby delineating new options for selective modulation of ER\u03b1.<\/jats:p>","DOI":"10.2337\/db13-0282","type":"journal-article","created":{"date-parts":[[2013,7,31]],"date-time":"2013-07-31T22:28:12Z","timestamp":1375309692000},"page":"4098-4108","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":116,"title":["Prevention of Obesity and Insulin Resistance by Estrogens Requires ER\u03b1 Activation Function-2 (ER\u03b1AF-2), Whereas ER\u03b1AF-1 Is Dispensable"],"prefix":"10.2337","volume":"62","author":[{"given":"Sandra","family":"Handgraaf","sequence":"first","affiliation":[{"name":"INSERM U1048, Institut des Maladies M\u00e9taboliques et Cardiovasculaires, Universit\u00e9 Toulouse III, 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