{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T13:24:22Z","timestamp":1785763462222,"version":"3.56.0"},"reference-count":72,"publisher":"Bioscientifica","issue":"3","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2018,12]]},"abstract":"<jats:p>\n                    Adipokine leptin regulates neuroendocrine circuits that control energy expenditure, thermogenesis and weight loss. However, canonic regulators of leptin secretion, such as insulin and malonyl CoA, do not support these processes. We hypothesize that epiregulin (EREG), a growth factor that is secreted from fibroblasts under thermogenic and cachexia conditions, induces leptin secretion associated with energy dissipation. The effects of EREG on leptin secretion were studied\n                    <jats:italic>ex vivo<\/jats:italic>\n                    , in the intra-abdominal white adipose tissue (iAb WAT) explants, as well as\n                    <jats:italic>in vivo<\/jats:italic>\n                    , in WT mice with diet-induced obesity (DIO) and in\n                    <jats:italic>ob\/ob<\/jats:italic>\n                    mice. These mice were pair fed a high-fat diet and treated with intraperitoneal injections of EREG. EREG increased leptin production and secretion in a dose-dependent manner in iAb fat explants via the EGFR\/MAPK pathway. After 2 weeks, the plasma leptin concentration was increased by 215% in the EREG-treated group compared to the control DIO group. EREG-treated DIO mice had an increased metabolic rate and core temperature during the active dark cycle and displayed cold-induced thermogenesis. EREG treatment reduced iAb fat mass, the major site of leptin protein production and secretion, but did not reduce the mass of the other fat depots. In the iAb fat, expression of genes supporting mitochondrial oxidation and thermogenesis was increased in EREG-treated mice vs control DIO mice. All metabolic and gene regulation effects of EREG treatment were abolished in leptin-deficient\n                    <jats:italic>ob\/ob<\/jats:italic>\n                    mice. Our data revealed a new role of EREG in induction of leptin secretion leading to the energy expenditure state. EREG could be a potential target protein to regulate hypo- and hyperleptinemia, underlying metabolic and immune diseases.\n                  <\/jats:p>","DOI":"10.1530\/joe-18-0289","type":"journal-article","created":{"date-parts":[[2018,11,1]],"date-time":"2018-11-01T19:13:41Z","timestamp":1541099621000},"page":"377-388","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-5","source":"Crossref","is-referenced-by-count":8,"title":["Epiregulin induces leptin secretion and energy expenditure in high-fat diet-fed mice"],"prefix":"10.1530","volume":"239","author":[{"given":"Rumana","family":"Yasmeen","sequence":"first","affiliation":[{"name":"1Department of Human Sciences, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiwen","family":"Shen","sequence":"additional","affiliation":[{"name":"1Department of Human Sciences, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aejin","family":"Lee","sequence":"additional","affiliation":[{"name":"1Department of Human Sciences, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacob H","family":"Leung","sequence":"additional","affiliation":[{"name":"1Department of Human Sciences, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Devan","family":"Kowdley","sequence":"additional","affiliation":[{"name":"1Department of Human Sciences, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David J","family":"DiSilvestro","sequence":"additional","affiliation":[{"name":"1Department of Human Sciences, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lu","family":"Xu","sequence":"additional","affiliation":[{"name":"1Department of Human Sciences, The Ohio State University, Columbus, Ohio, USA"},{"name":"2Department of Minimally Invasive Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kefeng","family":"Yang","sequence":"additional","affiliation":[{"name":"1Department of Human Sciences, The Ohio State University, Columbus, Ohio, USA"},{"name":"3Department of Nutrition, School of Medicine, Shanghai Jiao Tong University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrei","family":"Maiseyeu","sequence":"additional","affiliation":[{"name":"4Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naresh C","family":"Bal","sequence":"additional","affiliation":[{"name":"5Department of Physiology and Cell Biology, The Ohio State University, Columbus, Ohio, USA"},{"name":"6KIIT School of Biotechnology, KIIT University, Bhubaneswar, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Muthu","family":"Periasamy","sequence":"additional","affiliation":[{"name":"5Department of Physiology and Cell Biology, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paolo","family":"Fadda","sequence":"additional","affiliation":[{"name":"7Nucleic Acid Shared Resource, Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ouliana","family":"Ziouzenkova","sequence":"additional","affiliation":[{"name":"1Department of Human Sciences, The Ohio State University, Columbus, Ohio, 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