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In this study conducted on obese mice, we have explored: 1) CMKLR1 expression in the ileums; 2) CMKLR1 inhibitor \u03b1-NETA on body weight and intestinal mucosa integrity hence the impact on hepatic steatosis and pathway involved.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Nineteen male C57BL\/6 mice were randomly divided into five groups: normal diet group (ND), high-fat diet group (HFD), HFD\u2009+\u2009\u03b1-NETA group (NETA), HFD\u2009+\u2009PD98059 group (PD) and HFD\u2009+\u2009\u03b1-NETA\u2009+\u2009PD98059 group (NETA\u2009+\u2009PD). Mice were fed either with a chow diet or HFD for 12\u00a0weeks. At 12<jats:sup>th<\/jats:sup> week, mice of ND were put on the diet as before; mice of NETA received daily treatments of \u03b1-NETA (30\u00a0mg\/kg) via gavage; mice of PD received daily treatment of PD98059 via tail vein injection; mice of NETA\u2009+\u2009PD received daily treatment of \u03b1-NETA\u2009+\u2009PD98059, all for another 4\u00a0weeks. At the time intervention ended, mice were sacrificed. The body weight, the liver pathologies were assessed. Ileal CMKLR1 mRNA was evaluated by rtPCR; ZO-1, ERK1\/2 protein expression of ileal tissues by western blotting; liver TNF-\u03b1 and serum endotoxin by Elisa.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>More weight gains in mice of HFD than ND (37.90\u2009\u00b1\u20093.00\u00a0g) vs (24.47\u2009\u00b1\u20090.50\u00a0g), <jats:italic>P<\/jats:italic>\u2009=\u20090.002; \u03b1-NETA reduced the body weight (33.22\u2009\u00b1\u20091.90\u00a0g) vs (37.90\u2009\u00b1\u20093.00\u00a0g), <jats:italic>P<\/jats:italic>\u2009=\u20090.033; and further reduced by NETA\u2009+\u2009PD98059: (31.20\u2009\u00b1\u20091.74\u00a0g) vs (37.30\u2009\u00b1\u20094.05\u00a0g), <jats:italic>P<\/jats:italic>\u2009=\u20090.032. CMKLR1 mRNA expression was up-regulated in ileum in group HFD compared with ND and down-regulated by \u03b1-NETA. Steatosis was only alleviated in group PD\u2009+\u2009NETA with less weight gain. No impact of \u03b1-NETA on ileal ZO-1 or pERK with western blotting, and no endotoxin level changes were detected. TNF-\u03b1 was higher in group HFD than in group ND, while no significant difference between other groups.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>CMKLR1 mRNA was up-regulated in the ileum of obese mice and down-regulated by \u03b1-NETA along with a body weight control collaborating with ERK inhibitor PD98059. Steatosis was alleviated in a weight dependent way. \u03b1-NETA has no influence on intestinal mucosal integrity and no impact on steatohepatitis progression.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12902-023-01267-9","type":"journal-article","created":{"date-parts":[[2023,1,10]],"date-time":"2023-01-10T03:02:58Z","timestamp":1673319778000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["\u03b1-NETA down-regulates CMKLR1 mRNA expression in ileum and prevents body weight gains collaborating with ERK inhibitor PD98059 in turn to alleviate hepatic steatosis in HFD-induced obese mice but no impact on ileal mucosal integrity and steatohepatitis progression"],"prefix":"10.1186","volume":"23","author":[{"given":"Canbin","family":"Zheng","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yongping","family":"Zheng","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xi","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xianyang","family":"Zhong","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaobin","family":"Zheng","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shuhui","family":"Yang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zihui","family":"Zheng","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2023,1,10]]},"reference":[{"issue":"11","key":"1267_CR1","doi-asserted-by":"publisher","first-page":"300060521105684","DOI":"10.1177\/03000605211056841.PMCID:PMC8593317","volume":"49","author":"F T\u00fcrker","year":"2021","unstructured":"T\u00fcrker F, Oral A, \u015eahin T, et al. 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