{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T19:32:40Z","timestamp":1792006360249,"version":"4.4.0"},"reference-count":47,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","license":[{"start":{"date-parts":[[2022,1,11]],"date-time":"2022-01-11T00:00:00Z","timestamp":1641859200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatol Commun"],"published-print":{"date-parts":[[2022,6]]},"abstract":"<jats:p>\n                    Transforming growth factor beta (TGF\u2010\u03b2) signaling in hepatocytes promotes steatosis and body weight gain. However, processes that TGF\u2010\u03b2 signaling in hepatocytes promote pathological body weight gain in nonalcoholic fatty liver disease (NAFLD) are incompletely understood. Obesity and NAFLD were induced by 16\u00a0weeks of feeding a high\u2010fat diet (HFD) in hepatocyte\u2010specific TGF\u2010\u03b2 receptor II\u2013deficient (\n                    <jats:italic toggle=\"yes\">Tgfbr2\u0394HEP<\/jats:italic>\n                    ) and\n                    <jats:italic toggle=\"yes\">Tgfbr2flox\/flox<\/jats:italic>\n                    mice. In addition, browning of white adipose tissue (WAT) was induced by administration of CL\u2010316,243 (a \u03b23\u2010adrenergic agonist) or cold exposure for 7\u00a0days. Compared with\n                    <jats:italic toggle=\"yes\">Tgfbr2 flox\/flox<\/jats:italic>\n                    mice,\n                    <jats:italic toggle=\"yes\">Tgfbr2\u0394HEP<\/jats:italic>\n                    mice were resistant to steatosis and obesity. The metabolic changes in\n                    <jats:italic toggle=\"yes\">Tgfbr2\u0394HEP<\/jats:italic>\n                    mice were due to the increase of mitochondrial oxidative phosphorylation in the liver and white\u2010to\u2010beige fat conversion. A further mechanistic study revealed that exosomal let\u20107b\u20105p derived from hepatocytes was robustly elevated after stimulation with palmitic acid and TGF\u2010\u03b2. Indeed, let\u20107b\u20105p levels were low in the liver, serum exosomes, inguinal WAT, and epididymal WAT in HFD\u2010fed\n                    <jats:italic toggle=\"yes\">Tgfbr2\u0394HEP<\/jats:italic>\n                    mice. Moreover, 3T3\u2010L1 cells internalized hepatocyte\u2010derived exosomes. An\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    experiment demonstrated that let\u20107b\u20105p overexpression increased hepatocyte fatty acid transport and inhibited adipocyte\u2010like cell thermogenesis, whereas let\u20107b\u20105p inhibitor exerted the opposite effects.\n                    <jats:italic toggle=\"yes\">Conclusion:<\/jats:italic>\n                    Hepatocyte TGF\u2010\u03b2\u2010let\u20107b\u20105p signaling promotes HFD\u2010induced steatosis and obesity by reducing mitochondrial oxidative phosphorylation and suppressing white\u2010to\u2010beige fat conversion. This effect of hepatocyte TGF\u2010\u03b2 signaling in metabolism is partially associated with exosomal let\u20107b\u20105p.\n                  <\/jats:p>","DOI":"10.1002\/hep4.1892","type":"journal-article","created":{"date-parts":[[2022,1,12]],"date-time":"2022-01-12T02:39:46Z","timestamp":1641955186000},"page":"1301-1321","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":44,"title":["Hepatocyte TGF\u2010\u03b2 Signaling Inhibiting WAT Browning to Promote NAFLD and Obesity Is Associated With Let\u20107b\u20105p"],"prefix":"10.1097","volume":"6","author":[{"given":"Jinfang","family":"Zhao","sequence":"first","affiliation":[{"name":"Division of Gastroenterology,Union Hospital,Tongji Medical College,Huazhong University of Science and 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