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Review
. 2015 May 5;7(5):3219-39.
doi: 10.3390/nu7053219.

Can Skin Exposure to Sunlight Prevent Liver Inflammation?

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Free PMC article
Review

Can Skin Exposure to Sunlight Prevent Liver Inflammation?

Shelley Gorman et al. Nutrients. .
Free PMC article

Abstract

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.

Figures

Figure 1
Figure 1
Skin exposure to ultraviolet (UV) photons from sunlight results in the synthesis of effector molecules that modulate immune and metabolic processes. These include: skin release of nitric oxide (NO), increasing serum levels of nitrite; initiation of the conversion of precursor molecules such as reactive oxygen species (ROS), trans-urocanic acid (UCA) and 7-dehydrocholesterol (7-DHC) into platelet-activating factor, cis-UCA and 1,25-dihydroxyvitamin D (1,25(OH)2D, calcitriol), respectively; and, the release of heme oxygenase, neuropeptides and neurohormones (e.g., α-melanocyte stimulating hormone (α-MSH), nerve growth factor (NGF)), immunoregulatory (interleukin(IL)s-4 and -10) and pro-inflammatory (tumor necrosis factor-α, IL-1α, prostaglandins) cytokines. Sun exposure of the skin results in systemic production of active vitamin D (1,25(OH)2D) through hydroxylation of vitamin D in the liver and 25-hydroxyvitamin D (25(OH)D) in the kidneys. These events can also occur locally in skin and immune cells that express the hydroxylating enzymes.
Figure 2
Figure 2
Vitamin D may limit the progression of non-alcoholic fatty liver disease through multiple, potentially interacting mechanisms.

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References

    1. LaBrecque D., Anania F., Ferenci P., Ghafoor Khan A., Goh K.-L., Hamid S.S., Isakov V., Lizarzabal M., Mojica Pernaranda M., Rivera Ramos J.F., et al. Nonalcoholic Fatty Liver Disease and Nonalcholic Steatohepatitis. World Gastroenterology Organisation; Milwaukee, WI, USA: 2012.
    1. Berlanga A., Guiu-Jurado E., Porras J.A., Auguet T. Molecular pathways in non-alcoholic fatty liver disease. Clin. Exp. Gastroent. 2014;7:221–239. - PMC - PubMed
    1. Lade A., Noon L.A., Friedman S.L. Contributions of metabolic dysregulation and inflammation to nonalcoholic steatohepatitis, hepatic fibrosis, and cancer. Curr. Opin. Oncol. 2014;26:100–107. doi: 10.1097/CCO.0000000000000042. - DOI - PMC - PubMed
    1. Day C.P., James O.F. Steatohepatitis: A tale of two “hits”? Gastroenterology. 1998;114:842–845. doi: 10.1016/S0016-5085(98)70599-2. - DOI - PubMed
    1. Feldstein A.E., Werneburg N.W., Canbay A., Guicciardi M.E., Bronk S.F., Rydzewski R., Burgart L.J., Gores G.J. Free fatty acids promote hepatic lipotoxicity by stimulating tnf-alpha expression via a lysosomal pathway. Hepatology. 2004;40:185–194. doi: 10.1002/hep.20283. - DOI - PubMed

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