{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T17:46:00Z","timestamp":1791049560585,"version":"4.1.0"},"reference-count":57,"publisher":"Portland Press Ltd.","issue":"3","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2011,12,15]]},"abstract":"<jats:p>Adiponectin is protective against hepatic fibrosis, whereas leptin promotes fibrosis. In HSCs (hepatic stellate cells), leptin signals via a JAK2 (Janus kinase 2)\/STAT3 (signal transducer and activator of transcription 3) pathway, producing effects that enhance ECM (extracellular matrix) deposition. SOCS-3 (suppressor of cytokine signalling-3) and PTP1B (protein tyrosine phosphatase 1B) are both negative regulators of JAK\/STAT signalling, and recent studies have demonstrated a role for adiponectin in regulating SOCS-3 expression. In the present study we investigate mechanisms whereby adiponectin dampens leptin signalling and prevents excess ECM production. We treated culture-activated rat HSCs with recombinant adiponectin, leptin, both or neither, and also treated adiponectin knockout (Ad\u2212\/\u2212) and wild-type mice with leptin and\/or carbon tetrachloride (CCl4) or saline. We analyse JAK2 and Ob-Rb (long form of the leptin receptor) phosphorylation, and PTP1B expression and activity. We also explore potential mechanisms through which adiponectin regulates SOCS-3\u2013Ob-Rb association. Adiponectin inhibits leptin-stimulated JAK2 activation and Ob-Rb phosphorylation in HSCs, whereas both were increased in Ad\u2212\/\u2212 mice. Adiponectin stimulates PTP1B expression and activity in vitro, whereas PTP1B expression was lower in Ad\u2212\/\u2212mice than in wild-type mice. Adiponectin also promotes SOCS-3\u2013Ob-R association and blocks leptin-stimulated formation of extracellular TIMP-1 (tissue inhibitor of metalloproteinases-1)\u2013MMP-1 (matrix metalloproteinase-1) complexes in vitro. These results suggest two novel mechanisms whereby adiponectin inhibits hepatic fibrosis: (i) by promoting binding of SOCS-3 to Ob-Rb, and (ii) by stimulating PTP1B expression and activity, thus inhibiting JAK2\/STAT3 signalling at multiple points.<\/jats:p>","DOI":"10.1042\/bj20102148","type":"journal-article","created":{"date-parts":[[2011,8,17]],"date-time":"2011-08-17T04:14:35Z","timestamp":1313554475000},"page":"385-395","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":85,"title":["Adiponectin inhibits leptin signalling via multiple mechanisms to exert protective effects against hepatic fibrosis"],"prefix":"10.1042","volume":"440","author":[{"given":"Jeffrey\u00a0A.","family":"Handy","sequence":"first","affiliation":[{"name":"Division of Digestive Diseases, Emory University Department of Medicine, Atlanta, GA 30322, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ping\u00a0P.","family":"Fu","sequence":"additional","affiliation":[{"name":"Division of Digestive Diseases, Emory University Department of Medicine, Atlanta, GA 30322, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pradeep","family":"Kumar","sequence":"additional","affiliation":[{"name":"Division of Digestive Diseases, Emory University Department of Medicine, Atlanta, GA 30322, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jamie\u00a0E.","family":"Mells","sequence":"additional","affiliation":[{"name":"Division of Digestive Diseases, Emory University Department of Medicine, Atlanta, GA 30322, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shvetank","family":"Sharma","sequence":"additional","affiliation":[{"name":"Division of Digestive Diseases, Emory University Department of Medicine, Atlanta, GA 30322, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Neeraj\u00a0K.","family":"Saxena","sequence":"additional","affiliation":[{"name":"Division of Digestive Diseases, Emory University Department of Medicine, Atlanta, GA 30322, U.S.A."},{"name":"Department of Hematology and Oncology, Winship Cancer Institute, Emory University, Atlanta, GA 30322, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank\u00a0A.","family":"Anania","sequence":"additional","affiliation":[{"name":"Division of Digestive Diseases, Emory University Department of Medicine, Atlanta, GA 30322, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2011,11,28]]},"reference":[{"key":"2021112215214218600_B1","doi-asserted-by":"crossref","first-page":"1655","DOI":"10.1053\/j.gastro.2008.03.003","article-title":"Mechanisms of hepatic fibrogenesis","volume":"134","author":"Friedman","year":"2008","journal-title":"Gastroenterology"},{"key":"2021112215214218600_B2","doi-asserted-by":"crossref","first-page":"413","DOI":"10.1055\/s-2007-991517","article-title":"Hepatic fibrogenesis","volume":"27","author":"Guo","year":"2007","journal-title":"Sem. 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