{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T04:44:37Z","timestamp":1772772277606,"version":"3.50.1"},"reference-count":61,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2022,6,11]],"date-time":"2022-06-11T00:00:00Z","timestamp":1654905600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Intl J Eating Disorders"],"published-print":{"date-parts":[[2022,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Adiponectin, which is secreted from adipose tissue, is a protein hormone. Although a large body of studies have found that circulating adiponectin levels increase in anorexia nervosa (AN) and caloric restriction, the effect of subtypes of AN and modifiers of adiponectin in AN are not yet known.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A systematic search of electronic databases was performed using the search terms \u201cadiponectin,\u201d \u201canorexia nervosa,\u201d and \u201ceating disorder\u201d up to January 2021. All studies published in peer\u2010reviewed journals, which included cases and control groups, were selected. The main outcome was the pooled standardized mean difference (SMD) in adiponectin levels between cases and controls, using the random\u2010effects model. Modifiers of SMD were tested via meta\u2010regression. Heterogeneity and publication bias were evaluated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Thirty\u2010four studies met all eligibility criteria. The total sample of AN participants (Hedges' <jats:italic>g<\/jats:italic>\u00a0=\u2009.765, <jats:italic>p<\/jats:italic>\u00a0&lt;\u2009.0001), and specifically the binge\u2010eating\/purging (Hedges' <jats:italic>g<\/jats:italic>\u00a0=\u20091.211, <jats:italic>p<\/jats:italic>\u00a0&lt;\u2009.00001) and restrictive subtypes (Hedges' <jats:italic>g<\/jats:italic>\u00a0=\u2009.913, <jats:italic>p<\/jats:italic>\u00a0&lt;\u2009.00001) of AN have increased adiponectin plasma levels compared with healthy controls. Meta\u2010regression determined that insulin, IGF\u20101, BMI, triglyceride, resistin, glucose, IL\u20106 levels are significant modifiers of adiponectin levels.<\/jats:p><\/jats:sec><jats:sec><jats:title>Discussion<\/jats:title><jats:p>Compared with controls, adiponectin levels are higher in AN overall, and specifically in the binge\u2010eating\/purging and the restrictive AN subtypes. Many of metabolic parameters of glucose metabolism and pro\u2010inflammatory molecules modify the relationship between AN and adiponectin levels. Adipose tissue is important to maintain metabolic stability.<\/jats:p><\/jats:sec><jats:sec><jats:title>Public Significance<\/jats:title><jats:p>Anorexia nervosa is a psychiatric disorder associated with a severe decrease in body weight and multiple metabolic abnormalities, including an increase in the hormone adiponectin. In this paper, we used meta\u2010analysis, a powerful statistical method, to aggregate data from 34 rigorously selected research reports. This enabled us to understand the value of adiponectin to differentiate clinical subtypes of anorexia nervosa and the relations between adiponectin and other important metabolic parameters.<\/jats:p><\/jats:sec>","DOI":"10.1002\/eat.23753","type":"journal-article","created":{"date-parts":[[2022,6,11]],"date-time":"2022-06-11T11:44:32Z","timestamp":1654947872000},"page":"1279-1290","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Adiponectin in anorexia nervosa and its modifiers: A meta\u2010regression study"],"prefix":"10.1002","volume":"55","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1593-2180","authenticated-orcid":false,"given":"Umit","family":"Tural","sequence":"first","affiliation":[{"name":"Clinical Research Division The Nathan S. 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