{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T15:09:57Z","timestamp":1790435397622,"version":"4.1.0"},"reference-count":47,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2016,12,22]],"date-time":"2016-12-22T00:00:00Z","timestamp":1482364800000},"content-version":"vor","delay-in-days":356,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100003593","name":"Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico","doi-asserted-by":"publisher","award":["BJT 407352"],"award-info":[{"award-number":["BJT 407352"]}],"id":[{"id":"10.13039\/501100003593","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001822","name":"\u00d6sterreichischen Akademie der Wissenschaften","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001822","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2016,1]]},"abstract":"<jats:p><jats:italic>Background and Aims<\/jats:italic>. Angiotensin converting enzyme 2 (ACE2) is an important component of the renin\u2010angiotensin system. Since angiotensin peptides have been shown to be involved in hepatic steatosis, we aimed to evaluate the hepatic lipid profile in ACE2\u2010deficient (ACE2<jats:sup>\u2212\/y<\/jats:sup>) mice. <jats:italic>Methods<\/jats:italic>. Male C57BL\/6 and ACE2<jats:sup>\u2212\/y<\/jats:sup> mice were analyzed at the age of 3 and 6 months for alterations in the lipid profiles of plasma, faeces, and liver and for hepatic steatosis. <jats:italic>Results<\/jats:italic>. ACE2<jats:sup>\u2212\/y<\/jats:sup> mice showed lower body weight and white adipose tissue at all ages investigated. Moreover, these mice had lower levels of cholesterol, triglycerides, and nonesterified fatty acids in plasma. Strikingly, ACE2<jats:sup>\u2212\/y<\/jats:sup> mice showed high deposition of lipids in the liver. Expression of CD36, a protein involved in the uptake of triglycerides in liver, was increased in ACE2<jats:sup>\u2212\/y<\/jats:sup> mice. Concurrently, these mice exhibited an increase in hepatic oxidative stress, evidenced by increased lipid peroxidation and expression of uncoupling protein 2, and downregulation of sirtuin 1. ACE2<jats:sup>\u2212\/y<\/jats:sup> mice also showed impairments in glucose metabolism and insulin signaling in the liver. <jats:italic>Conclusions<\/jats:italic>. Deletion of ACE2 causes CD36\/sirtuin 1 axis impairment and thereby interferes with lipid homeostasis, leading to lipodystrophy and steatosis.<\/jats:p>","DOI":"10.1155\/2016\/6487509","type":"journal-article","created":{"date-parts":[[2016,12,23]],"date-time":"2016-12-23T17:50:58Z","timestamp":1482515458000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["CD36\/Sirtuin 1 Axis Impairment Contributes to Hepatic Steatosis in ACE2\u2010Deficient 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