{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:48:11Z","timestamp":1787014091843,"version":"build-2736575974"},"reference-count":19,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2017,7,10]],"date-time":"2017-07-10T00:00:00Z","timestamp":1499644800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2017,12]]},"abstract":"<jats:p>\n                    The beneficial effects of mineralocorticoid receptor blockade by spironolactone have been shown in animal models of non\u2010alcoholic fatty liver disease (\n                    <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content>\n                    ). The aim of the present 52\u2010week randomized controlled trial was to compare the effects of low\u2010dose spironolactone and vitamin E combination with those of vitamin E monotherapy on insulin resistance, non\u2010invasive indices of hepatic steatosis and fibrosis, liver function tests, circulating adipokines and hormones in patients with histologically confirmed\n                    <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content>\n                    . Homeostasis model of assessment of insulin resistance (\n                    <jats:styled-content style=\"fixed-case\">HOMA\u2010IR<\/jats:styled-content>\n                    ) and non\u2010invasive indices of steatosis and fibrosis were calculated. Analysis was intention\u2010to\u2010treat.\n                    <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content>\n                    liver fat score, an index of steatosis, decreased significantly in the combination treatment group (\n                    <jats:italic>P<\/jats:italic>\n                    = .028), but not in the vitamin E group, and the difference for group*time interaction was significant (\n                    <jats:italic>P<\/jats:italic>\n                    = .047). Alanine aminotransferase\u2010to\u2010platelet ratio index, an index of fibrosis, did not change. Insulin levels and\n                    <jats:styled-content style=\"fixed-case\">HOMA\u2010IR<\/jats:styled-content>\n                    decreased significantly only within the combination group (\n                    <jats:italic>P<\/jats:italic>\n                    = .011 and\n                    <jats:italic>P<\/jats:italic>\n                    = .011, respectively). In conclusion, the combined low\u2010dose spironolactone plus vitamin E regimen significantly decreased\n                    <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content>\n                    liver fat score. Larger\u2010scale trials are needed to clarify the effect of low\u2010dose spironolactone on hepatic histology.\n                  <\/jats:p>","DOI":"10.1111\/dom.12989","type":"journal-article","created":{"date-parts":[[2017,4,28]],"date-time":"2017-04-28T03:46:42Z","timestamp":1493351202000},"page":"1805-1809","source":"Crossref","is-referenced-by-count":76,"title":["Effects of combined low\u2010dose spironolactone plus vitamin E vs vitamin E monotherapy on insulin resistance, non\u2010invasive indices of steatosis and fibrosis, and adipokine levels in non\u2010alcoholic fatty liver disease:\n                    <scp>a<\/scp>\n                    randomized controlled trial"],"prefix":"10.1111","volume":"19","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9232-4042","authenticated-orcid":false,"given":"Stergios A.","family":"Polyzos","sequence":"first","affiliation":[{"name":"Second Medical Clinic, School of Medicine Aristotle University of Thessaloniki  Thessaloniki Greece"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jannis","family":"Kountouras","sequence":"additional","affiliation":[{"name":"Second Medical Clinic, School of Medicine Aristotle University of Thessaloniki  Thessaloniki Greece"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christos S.","family":"Mantzoros","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism Beth Israel Deaconess Medical Center, Harvard Medical School  Boston Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vaia","family":"Polymerou","sequence":"additional","affiliation":[{"name":"Department of Biopathology, Biomedicine Laboratories  Athens Greece"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Panagiotis","family":"Katsinelos","sequence":"additional","affiliation":[{"name":"Second Medical Clinic, School of Medicine Aristotle University of Thessaloniki  Thessaloniki 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