{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T01:31:07Z","timestamp":1791077467539,"version":"4.1.0"},"reference-count":26,"publisher":"American Diabetes Association","issue":"5","license":[{"start":{"date-parts":[[2021,9,1]],"date-time":"2021-09-01T00:00:00Z","timestamp":1630454400000},"content-version":"vor","delay-in-days":3787,"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":[[2011,5,1]]},"abstract":"<jats:sec>\n                    <jats:title>OBJECTIVE<\/jats:title>\n                    <jats:p>Type 2 diabetes is an established risk factor for development of hepatic steatosis and nonalcoholic fatty liver disease (NAFLD). We aimed to determine the prevalence and clinical correlates of these conditions in a large cohort of people with type 2 diabetes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESEARCH DESIGN AND METHODS<\/jats:title>\n                    <jats:p>A total of 939 participants, aged 61\u201376 years, from the Edinburgh Type 2 Diabetes Study (ET2DS)\u2014a large, randomly selected population of people with type 2 diabetes\u2014underwent liver ultrasonography. Ultrasound gradings of steatosis were compared with magnetic resonance spectroscopy in a subgroup. NAFLD was defined as hepatic steatosis in the absence of a secondary cause (screened by questionnaire assessing alcohol and hepatotoxic medication use, plasma hepatitis serology, autoantibodies and ferritin, and record linkage to determine prior diagnoses of liver disease). Binary logistic regression was used to analyze independent associations of characteristics with NAFLD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>Hepatic steatosis was present in 56.9% of participants. After excluding those with a secondary cause for steatosis, the prevalence of NAFLD in the study population was 42.6%. Independent predictors of NAFLD were BMI, lesser duration of diabetes, HbA1c, triglycerides, and metformin use. These remained unchanged after exclusion of participants with evidence of hepatic fibrosis from the group with no hepatic steatosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS<\/jats:title>\n                    <jats:p>Prevalences of hepatic steatosis and NAFLD were high in this unselected population of older people with type 2 diabetes, but lower than in studies in which ultrasound gradings were not compared with a gold standard. Associations with features of the metabolic syndrome could be used to target screening for this condition.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2337\/dc10-2229","type":"journal-article","created":{"date-parts":[[2011,4,9]],"date-time":"2011-04-09T00:02:14Z","timestamp":1302307334000},"page":"1139-1144","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":333,"title":["Prevalence of and Risk Factors for Hepatic Steatosis and Nonalcoholic Fatty Liver Disease in People With Type 2 Diabetes: the Edinburgh Type 2 Diabetes Study"],"prefix":"10.2337","volume":"34","author":[{"given":"Rachel M.","family":"Williamson","sequence":"first","affiliation":[{"name":"Metabolic Unit, Western General Hospital, Edinburgh, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jackie F.","family":"Price","sequence":"additional","affiliation":[{"name":"Centre for Population Health Sciences, The University of Edinburgh, Edinburgh, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen","family":"Glancy","sequence":"additional","affiliation":[{"name":"Department of Radiology, Western General Hospital, Edinburgh, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisa","family":"Perry","sequence":"additional","affiliation":[{"name":"Department of Radiology, Western General Hospital, Edinburgh, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa D.","family":"Nee","sequence":"additional","affiliation":[{"name":"Department of Radiology, Western General Hospital, Edinburgh, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter C.","family":"Hayes","sequence":"additional","affiliation":[{"name":"Department of Hepatology, Royal Infirmary of Edinburgh, Edinburgh, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian M.","family":"Frier","sequence":"additional","affiliation":[{"name":"Department of Diabetes, Royal Infirmary of Edinburgh, Edinburgh, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liesbeth A.F.","family":"Van Look","sequence":"additional","affiliation":[{"name":"Metabolic Unit, Western General Hospital, Edinburgh, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Geoffrey I.","family":"Johnston","sequence":"additional","affiliation":[{"name":"Pfizer Global R&D, Sandwich, Kent, U.K. and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebecca M.","family":"Reynolds","sequence":"additional","affiliation":[{"name":"Endocrinology Unit, University\/BHF Centre for Cardiovascular Science, University of Edinburgh, Queens Medical Research Institute, Edinburgh, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark W.J.","family":"Strachan","sequence":"additional","affiliation":[{"name":"Metabolic Unit, Western 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