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While the pathogenesis of lipid accumulation has been extensively studied, the protective mechanism against lipid challenge in the liver remains unclear. Here, we report that Src homology 3 domain binding kinase 1 (SBK1) is a regulator of hepatic lipid metabolism and systemic insulin sensitivity in response to obesity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Approach and Results:<\/jats:title>\n                    <jats:p>\n                      Enhanced\n                      <jats:italic toggle=\"yes\">Sbk1<\/jats:italic>\n                      expression was found in the liver of high\u2010fat diet (HFD)\u2013induced obese mice and fatty acid (FA)\u2013challenged hepatocytes.\n                      <jats:italic toggle=\"yes\">SBK1<\/jats:italic>\n                      knockdown in mouse liver cells augmented FA uptake and lipid accumulation. Similarly, liver\u2010specific\n                      <jats:italic toggle=\"yes\">SBK1<\/jats:italic>\n                      knockout (\n                      <jats:italic toggle=\"yes\">Lsko<\/jats:italic>\n                      ) mice displayed more severe hepatosteatosis and higher expression of genes in FA uptake and lipogenesis than the Flox\/Flox (\n                      <jats:italic toggle=\"yes\">Fl\/Fl<\/jats:italic>\n                      ) control mice when fed the HFD. The HFD\u2010fed\n                      <jats:italic toggle=\"yes\">Lsko<\/jats:italic>\n                      mice also showed symptoms of hyperglycemia, poor systemic glucose tolerance, and lower insulin sensitivity than the\n                      <jats:italic toggle=\"yes\">Fl\/Fl<\/jats:italic>\n                      mice. On the other hand, hepatic\n                      <jats:italic toggle=\"yes\">Sbk1<\/jats:italic>\n                      overexpression alleviated the high\u2010fructose diet\u2013induced hepatosteatosis, hyperlipidemia, and hyperglycemia in mice. White adipose tissue browning was also observed in hepatic\n                      <jats:italic toggle=\"yes\">SBK1<\/jats:italic>\n                      \u2010overexpressed mice. Moreover, we found that SBK1 was a positive regulator of FGF21 in the liver during energy surplus conditions. Mechanistically, SBK1 phosphorylates the orphan nuclear receptor 4A1 (Nur77) on serine 344 to promote hepatic\n                      <jats:italic toggle=\"yes\">FGF21<\/jats:italic>\n                      expression and inhibit the transcription of genes involved in lipid anabolism.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>Collectively, our data suggest that SBK1 is a regulator of the metabolic adaption against obesity through the Nur77\u2013FGF21 pathway.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/hep.32501","type":"journal-article","created":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T15:26:54Z","timestamp":1648826814000},"page":"213-229","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":25,"title":["Src homology 3 domain binding kinase 1 protects against hepatic steatosis and insulin resistance through the Nur77\u2013FGF21 pathway"],"prefix":"10.1097","volume":"77","author":[{"given":"Palak","family":"Ahuja","sequence":"first","affiliation":[{"name":"School of Biological Sciences, The University of Hong Kong, Hong Kong SAR, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xinyi","family":"Bi","sequence":"additional","affiliation":[{"name":"School of Biological Sciences, The University of Hong Kong, Hong Kong SAR, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chun Fai","family":"Ng","sequence":"additional","affiliation":[{"name":"School of Biological Sciences, The University of Hong Kong, Hong Kong SAR, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Margaret Chui Ling","family":"Tse","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences, The University of Hong Kong, Hong Kong SAR, 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