{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T19:05:43Z","timestamp":1790017543584,"version":"4.0.1"},"reference-count":68,"publisher":"eLife Sciences Publications, Ltd","license":[{"start":{"date-parts":[[2023,8,15]],"date-time":"2023-08-15T00:00:00Z","timestamp":1692057600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2023,8,15]],"date-time":"2023-08-15T00:00:00Z","timestamp":1692057600000},"content-version":"am","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2023,8,15]],"date-time":"2023-08-15T00:00:00Z","timestamp":1692057600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["81870586"],"award-info":[{"award-number":["81870586"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Hong Kong University Grants Committee, Area of Excellence","award":["AoE\/M-707\/18"],"award-info":[{"award-number":["AoE\/M-707\/18"]}]},{"name":"Hong Kong University Grants Committee, General Research Fund","award":["15101520"],"award-info":[{"award-number":["15101520"]}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["82270941"],"award-info":[{"award-number":["82270941"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["81974117"],"award-info":[{"award-number":["81974117"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["elifesciences.org"],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2023,7,28]]},"abstract":"<jats:sec id=\"abs1\">\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>\n                      Recent research has shown that the adhesion G protein-coupled receptor F1 (\n                      <jats:italic>Adgrf1;<\/jats:italic>\n                      also known as\n                      <jats:italic>GPR110; PGR19; KPG_012; hGPCR36<\/jats:italic>\n                      ) is an oncogene. The evidence is mainly based on high expression of\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      in numerous cancer types, and knockdown\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      can reduce the cell migration, invasion, and proliferation.\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      is, however, mostly expressed in the liver of healthy individuals. The function of\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      in liver has not been revealed. Interestingly, expression level of hepatic\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      is dramatically decreased in obese subjects. Here, the research examined whether\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      has a role in liver metabolism.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"abs2\">\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      We used recombinant adeno-associated virus-mediated gene delivery system, and antisense oligonucleotide was used to manipulate the hepatic\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      expression level in diet-induced obese mice to investigate the role of\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      in hepatic steatosis. The clinical relevance was examined using transcriptome profiling and archived biopsy specimens of liver tissues from non-alcoholic fatty liver disease (NAFLD) patients with different degree of fatty liver.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"abs3\">\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      The expression of\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      in the liver was directly correlated to fat content in the livers of both obese mice and NAFLD patients. Stearoyl-coA desaturase 1 (\n                      <jats:italic>Scd1<\/jats:italic>\n                      ), a crucial enzyme in hepatic de novo lipogenesis, was identified as a downstream target of\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      by RNA-sequencing analysis. Treatment with the liver-specific\n                      <jats:italic>Scd1<\/jats:italic>\n                      inhibitor MK8245 and specific shRNAs against\n                      <jats:italic>Scd1<\/jats:italic>\n                      in primary hepatocytes improved the hepatic steatosis of\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      -overexpressing mice and lipid profile of hepatocytes, respectively.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"abs4\">\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>\n                      These results indicate\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      regulates hepatic lipid metabolism through controlling the expression of\n                      <jats:italic>Scd1<\/jats:italic>\n                      . Downregulation of\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      expression can potentially serve as a protective mechanism to stop the overaccumulation of fat in the liver in obese subjects. Overall, the above findings not only reveal a new mechanism regulating the progression of NAFLD, but also proposed a novel therapeutic approach to combat NAFLD by targeting\n                      <jats:italic>Adgrf1<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"abs5\">\n                    <jats:title>Funding:<\/jats:title>\n                    <jats:p>This work was supported by the National Natural Science Foundation of China (81870586), Area of Excellence (AoE\/M-707\/18), and General Research Fund (15101520) to CMW, and the National Natural Science Foundation of China (82270941, 81974117) to SJ.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.7554\/elife.85131","type":"journal-article","created":{"date-parts":[[2023,8,2]],"date-time":"2023-08-02T07:15:13Z","timestamp":1690960513000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.85131","source":"Crossref","is-referenced-by-count":19,"title":["Amelioration of non-alcoholic fatty liver disease by targeting adhesion G protein-coupled receptor F1 (Adgrf1)"],"prefix":"10.7554","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5748-5780","authenticated-orcid":true,"given":"Mengyao","family":"Wu","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05ar8rn06","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Chemistry and Chemical Engineering, Guangzhou University","place":["Guangzhou, 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