{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T08:38:47Z","timestamp":1778661527181,"version":"3.51.4"},"reference-count":104,"publisher":"MDPI AG","issue":"5","license":[{"start":{"date-parts":[[2015,5,5]],"date-time":"2015-05-05T00:00:00Z","timestamp":1430784000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nutrients"],"abstract":"<jats:p>Liver inflammation contributes towards the pathology of non-alcoholic fatty liver disease (NAFLD). Here we discuss how skin exposure to sunlight may suppress liver inflammation and the severity of NAFLD. Following exposure to sunlight-derived ultraviolet radiation (UVR), the skin releases anti-inflammatory mediators such as vitamin D and nitric oxide. Animal modeling studies suggest that exposure to UVR can prevent the development of NAFLD. Association studies also support a negative link between circulating 25-hydroxyvitamin D and NAFLD incidence or severity. Clinical trials are in their infancy and are yet to demonstrate a clear beneficial effect of vitamin D supplementation. There are a number of potentially interdependent mechanisms whereby vitamin D could dampen liver inflammation, by inhibiting hepatocyte apoptosis and liver fibrosis, modulating the gut microbiome and through altered production and transport of bile acids. While there has been a focus on vitamin D, other mediators induced by sun exposure, such as nitric oxide may also play important roles in curtailing liver inflammation.<\/jats:p>","DOI":"10.3390\/nu7053219","type":"journal-article","created":{"date-parts":[[2015,5,5]],"date-time":"2015-05-05T10:43:16Z","timestamp":1430822596000},"page":"3219-3239","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Can Skin Exposure to Sunlight Prevent Liver Inflammation?"],"prefix":"10.3390","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7111-6735","authenticated-orcid":false,"given":"Shelley","family":"Gorman","sequence":"first","affiliation":[{"name":"Telethon Kids Institute, University of Western Australia, 100 Roberts Rd, Subiaco, Western Australia 6008, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucinda","family":"Black","sequence":"additional","affiliation":[{"name":"Telethon Kids Institute, University of Western Australia, 100 Roberts Rd, Subiaco, Western Australia 6008, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2320-1158","authenticated-orcid":false,"given":"Martin","family":"Feelisch","sequence":"additional","affiliation":[{"name":"Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton General Hospital, Southampton, SO16 6YD, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Prue","family":"Hart","sequence":"additional","affiliation":[{"name":"Telethon Kids Institute, University of Western Australia, 100 Roberts Rd, Subiaco, Western Australia 6008, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard","family":"Weller","sequence":"additional","affiliation":[{"name":"University of Edinburgh, MRC Centre for Inflammation Research, Edinburgh, EH16 4TJ, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2015,5,5]]},"reference":[{"key":"ref_1","unstructured":"LaBrecque, D., Anania, F., Ferenci, P., Ghafoor Khan, A., Goh, K.-L., Hamid, S.S., Isakov, V., Lizarzabal, M., Mojica Pernaranda, M., and Rivera Ramos, J.F. 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