{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:20:57Z","timestamp":1784557257417,"version":"3.55.0"},"reference-count":0,"publisher":"Bioscientifica","issue":"2","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2021,2]]},"abstract":"<jats:p>\n                    Oxidative stress is proposed to be involved in nonalcoholic fatty liver disease (NAFLD). However, antioxidant therapy results in controversial outcomes. Therefore, we generated a new antioxidant\/NAFLD mouse model,\n                    <jats:italic>\n                      Lias\n                      <jats:sup>High\/High<\/jats:sup>\n                      Lepr\n                      <jats:sup>db\/db<\/jats:sup>\n                    <\/jats:italic>\n                    mice, by crossbreeding\n                    <jats:italic>\n                      Lepr\n                      <jats:sup>db\/db<\/jats:sup>\n                    <\/jats:italic>\n                    mice, an obesity mouse model, with\n                    <jats:italic>\n                      Lias\n                      <jats:sup>High\/High<\/jats:sup>\n                    <\/jats:italic>\n                    mice, generated by overexpression of lipoic acid synthase gene (\n                    <jats:italic>Lias<\/jats:italic>\n                    ) and having increased endogenous antioxidant capacity, to investigate whether the new model could block the development of NAFLD. We have systemically characterized the novel model based on the main features of human NAFLD, determined the impact of enhanced endogenous antioxidant capacity on the retardation of NAFLD and elucidated the underlying mechanisms using various biological and pathological methods. We found that\n                    <jats:italic>\n                      Lias\n                      <jats:sup>High\/High<\/jats:sup>\n                      Lepr\n                      <jats:sup>db\/db<\/jats:sup>\n                    <\/jats:italic>\n                    mice ameliorated many pathological changes of NAFLD compared with the control. In particular,\n                    <jats:italic>\n                      Lias\n                      <jats:sup>High\/High<\/jats:sup>\n                      Lepr\n                      <jats:sup>db\/db<\/jats:sup>\n                    <\/jats:italic>\n                    mice displayed the improved liver mitochondrial function, reflecting the decline of mitochondrial microvesicular steatosis, and reduced oxidative stress, which mainly contributes to the alleviation of pathologic alterations of the NAFLD progression. Our new model shows that mitochondrial dysfunction is a major pathogenesis for liver steatosis. Overexpression of\n                    <jats:italic>Lias<\/jats:italic>\n                    gene effectively reduces oxidative stress and protects mitochondria, and consequently attenuates NAFLD\/NASH.\n                  <\/jats:p>","DOI":"10.1530\/joe-19-0606","type":"journal-article","created":{"date-parts":[[2020,12,2]],"date-time":"2020-12-02T10:51:54Z","timestamp":1606906314000},"page":"119-131","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-5","source":"Crossref","is-referenced-by-count":13,"title":["Overexpression of the Lias gene attenuates hepatic steatosis in Leprdb\/db mice"],"prefix":"10.1530","volume":"248","author":[{"given":"Guangcui","family":"Xu","sequence":"first","affiliation":[{"name":"1School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tingting","family":"Yan","sequence":"additional","affiliation":[{"name":"1School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiang","family":"Peng","sequence":"additional","affiliation":[{"name":"1School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haibin","family":"Li","sequence":"additional","affiliation":[{"name":"1School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weidong","family":"Wu","sequence":"additional","affiliation":[{"name":"1School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xianwen","family":"Yi","sequence":"additional","affiliation":[{"name":"2Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yingzheng","family":"Zhao","sequence":"additional","affiliation":[{"name":"1School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","container-title":["Journal of Endocrinology"],"original-title":[],"link":[{"URL":"https:\/\/joe.bioscientifica.com\/view\/journals\/joe\/248\/2\/JOE-19-0606.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/joe.bioscientifica.com\/downloadpdf\/journals\/joe\/248\/2\/JOE-19-0606.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T13:57:06Z","timestamp":1784555826000},"score":1,"resource":{"primary":{"URL":"http:\/\/journals.bioscientifica.com\/joe\/article\/248\/2\/119-131\/5468"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2021,2]]},"references-count":0,"journal-issue":{"issue":"2"},"URL":"https:\/\/doi.org\/10.1530\/joe-19-0606","relation":{},"ISSN":["0022-0795","1479-6805"],"issn-type":[{"value":"0022-0795","type":"print"},{"value":"1479-6805","type":"electronic"}],"subject":[],"published":{"date-parts":[[2021,2]]}}}