{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,10]],"date-time":"2026-01-10T01:22:10Z","timestamp":1768008130937,"version":"3.49.0"},"reference-count":44,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","license":[{"start":{"date-parts":[[2017,6,27]],"date-time":"2017-06-27T00:00:00Z","timestamp":1498521600000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2017,8]]},"abstract":"<jats:p>Cholesterol synthesis is regulated by the transcription factor sterol regulatory element binding protein 2 (SREBP\u20102) and its target gene 3\u2010hydroxy\u20103\u2010methylglutaryl\u2010coenzyme A reductase (HMGCR), which is the rate\u2010limiting enzyme in cholesterol synthesis. Cyclic adenosine monophosphate\u2013responsive element (CRE) binding protein\u2013regulated transcription coactivator (CRTC) 2 is the master regulator of glucose metabolism. However, the effect of CRTC2 on cholesterol and its potential molecular mechanism remain unclear. Here, we demonstrated that CRTC2 expression and liver cholesterol content were increased in patients with high serum cholesterol levels who underwent resection of liver hemangiomas, as well as in mice fed a 4% cholesterol diet. Mice with adenovirus\u2010mediated CRTC2 overexpression also showed elevated lipid levels in both serum and liver tissues. Intriguingly, hepatic <jats:italic toggle=\"yes\">de novo<\/jats:italic> cholesterol synthesis was markedly increased under these conditions. In contrast, CRTC2 ablation in mice fed a 4% cholesterol diet (18 weeks) showed decreased lipid levels in serum and liver tissues compared with those in littermate wild\u2010type mice. The expression of lipogenic genes (SREBP\u20102 and HMGCR) was consistent with hepatic CRTC2 levels. <jats:italic toggle=\"yes\">In vivo<\/jats:italic> imaging showed enhanced adenovirus\u2010mediated HMGCR\u2010luciferase activity in adenovirus\u2010mediated CRTC2 mouse livers; however, the activity was attenuated after mutation of CRE or sterol regulatory element sequences in the HMGCR reporter construct. The effect of CRTC2 on HMGCR in mouse livers was alleviated upon SREBP\u20102 knockdown. CRTC2 modulated SREBP\u20102 transcription by CRE binding protein, which recognizes the half\u2010site CRE sequence in the SREBP\u20102 promoter. CRTC2 reduced the nuclear protein expression of forkhead box O1 and subsequently increased SREBP\u20102 transcription by binding insulin response element 1, rather than insulin response element 2, in the SREBP\u20102 promoter. <jats:italic toggle=\"yes\">Conclusion<\/jats:italic>: CRTC2 regulates the transcription of SREBP\u20102 by interfering with the recognition of insulin response element 1 in the SREBP\u20102 promoter by forkhead box O1, thus inducing SREBP\u20102\/HMGCR signaling and subsequently facilitating hepatic cholesterol synthesis. (H<jats:sc>epatology<\/jats:sc> 2017;66:481\u2013497).<\/jats:p>","DOI":"10.1002\/hep.29206","type":"journal-article","created":{"date-parts":[[2017,4,10]],"date-time":"2017-04-10T16:32:39Z","timestamp":1491841959000},"page":"481-497","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":38,"title":["A novel role for CRTC2 in hepatic cholesterol synthesis through SREBP\u20102"],"prefix":"10.1097","volume":"66","author":[{"given":"Yujie","family":"Li","sequence":"first","affiliation":[{"name":"Department of Endocrinology,Shandong Provincial Hospital Affiliated to Shandong University,Shandong,China"},{"name":"Shandong Clinical Medical Center of Endocrinology and Metabolism,Shandong,China"},{"name":"Institute of Endocrinology and Metabolism,Shandong Academy of Clinical 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