{"id":80176,"date":"2025-03-18T11:55:40","date_gmt":"2025-03-18T02:55:40","guid":{"rendered":"https:\/\/www.waseda.jp\/inst\/research\/?p=80176"},"modified":"2025-03-18T14:10:37","modified_gmt":"2025-03-18T05:10:37","slug":"liver-derived-neuregulin-1%ce%b1-stimulates-compensatory-pancreatic-%ce%b2-cell-hyperplasia-in-insulin-resistance%ef%bc%88published-in-nature-communications-march-2025%ef%bc%89","status":"publish","type":"post","link":"https:\/\/www.waseda.jp\/inst\/research\/news\/80176","title":{"rendered":"Liver-derived Neuregulin 1\u03b1 stimulates compensatory pancreatic \u03b2 cell hyperplasia in insulin resistance\uff08Published in Nature Communications, March, 2025\uff09"},"content":{"rendered":"<table class=\"table table-bordered table-colored-tbhd\" style=\"height: 550px; width: 100%; border-collapse: collapse; border-style: solid;\" border=\"1\">\n<tbody>\n<tr style=\"height: 78px;\">\n<td style=\"width: 19.0523%; height: 78px;\">Journal Title<br \/>\n\/\u63b2\u8f09\u30b8\u30e3\u30fc\u30ca\u30eb\u540d<\/td>\n<td style=\"width: 80.849%; height: 78px;\">Nature Communications<\/td>\n<\/tr>\n<tr style=\"height: 65px;\">\n<td style=\"width: 19.0523%; height: 80px;\">Publication Year and Month<br \/>\n\/\u63b2\u8f09\u5e74\u6708<\/td>\n<td style=\"width: 80.849%; height: 80px;\">March, 2025<\/td>\n<\/tr>\n<tr style=\"height: 55px;\">\n<td style=\"width: 19.0523%; height: 79px;\">Paper Title<br \/>\n\/\u8ad6\u6587\u30bf\u30a4\u30c8\u30eb<\/td>\n<td style=\"width: 80.849%; height: 79px;\">Liver-derived Neuregulin 1\u03b1 stimulates compensatory pancreatic \u03b2 cell hyperplasia in insulin resistance<\/td>\n<\/tr>\n<tr style=\"height: 85px;\">\n<td style=\"width: 19.0523%; height: 85px;\">DOI<br \/>\n\/\u8ad6\u6587DOI<\/td>\n<td style=\"width: 80.849%; height: 85px;\"><a href=\"https:\/\/doi.org\/10.1038\/S41467-025-57167-0\">10.1038\/S41467-025-57167-0<\/a><\/td>\n<\/tr>\n<tr style=\"height: 59px;\">\n<td style=\"width: 19.0523%; height: 80px;\">\u00a0Author of Waseda University<br \/>\n\/\u672c\u5b66\u306e\u8457\u8005<\/td>\n<td style=\"width: 80.849%; height: 80px;\"><span style=\"font-family: inherit; font-size: inherit;\">GODA, Nobuhito(Professor, Faculty of Science and Engineering, School of Advanced Science and Engineering):Correspoinding Author<\/span><\/td>\n<\/tr>\n<tr style=\"height: 68px;\">\n<td style=\"width: 19.0523%; height: 86px;\">Related Websites<br \/>\n\/\u95a2\u9023Web<\/td>\n<td style=\"width: 80.849%; height: 86px;\">&#8211;<\/td>\n<\/tr>\n<tr style=\"height: 138px;\">\n<td style=\"width: 19.0523%; height: 148px;\">Abstract<br \/>\n\/\u6284\u9332<\/td>\n<td style=\"width: 80.849%; height: 148px;\">Compensatory pancreatic islet hyperplasia is an adaptive response to increased systemic insulin demand, although factors meditating this response remain poorly understood. Here, we show that a liver-derived secreted protein, Neuregulin1\u03b1, promotes compensatory proliferation of pancreatic \u03b2 cells in type 2 diabetes. Liver\u00a0<i>Neuregulin1\u03b1<\/i>\u00a0expression and serum Neuregulin1\u03b1 levels increase in male mice fed an obesity-inducing diet. Male mice lacking either\u00a0<i>Neuregulin1<\/i>\u00a0in liver or its receptor,\u00a0<i>ErbB3<\/i>, in \u03b2 cells deteriorate systemic glucose disposal due to impaired \u03b2 cell expansion with reduced insulin secretion when fed the obesity-inducing diet. Mechanistically, Neuregulin1\u03b1 activates ERBB2\/3-ERK signaling to stimulate \u03b2 cell proliferation without altering glucose-stimulated insulin secretion potential. In patients with metabolic dysfunction-associated steatotic liver disease (MASLD) and obesity but without type 2 diabetes serum Neuregulin1\u03b1 levels increase, while in patient with MASLD and type 2 diabetes show markedly reduced levels of Neuregulin1\u03b1. These results suggest that Neuregulin1\u03b1 serves as a hepatokine that can expand functional \u03b2 cell mass in type 2 diabetes.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n","protected":false},"excerpt":{"rendered":"<p>Journal Title \/\u63b2\u8f09\u30b8\u30e3\u30fc\u30ca\u30eb\u540d Nature Communications Publication Year and Month \/\u63b2\u8f09\u5e74\u6708 March, 2025 Paper Title \/\u8ad6\u6587\u30bf\u30a4\u30c8\u30eb [&hellip;]<\/p>\n","protected":false},"author":3,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[],"tags":[218,217],"class_list":["post-80176","post","type-post","status-publish","format-standard","hentry","tag-impact-en","tag-impact"],"acf":[],"_links":{"self":[{"href":"https:\/\/www.waseda.jp\/inst\/research\/wp-json\/wp\/v2\/posts\/80176","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.waseda.jp\/inst\/research\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.waseda.jp\/inst\/research\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.waseda.jp\/inst\/research\/wp-json\/wp\/v2\/users\/3"}],"replies":[{"embeddable":true,"href":"https:\/\/www.waseda.jp\/inst\/research\/wp-json\/wp\/v2\/comments?post=80176"}],"version-history":[{"count":1,"href":"https:\/\/www.waseda.jp\/inst\/research\/wp-json\/wp\/v2\/posts\/80176\/revisions"}],"predecessor-version":[{"id":80193,"href":"https:\/\/www.waseda.jp\/inst\/research\/wp-json\/wp\/v2\/posts\/80176\/revisions\/80193"}],"wp:attachment":[{"href":"https:\/\/www.waseda.jp\/inst\/research\/wp-json\/wp\/v2\/media?parent=80176"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.waseda.jp\/inst\/research\/wp-json\/wp\/v2\/categories?post=80176"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.waseda.jp\/inst\/research\/wp-json\/wp\/v2\/tags?post=80176"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}