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Effects of vitamin D deficiency on chronic alcoholic liver injury

Vitamin D deficiency (VDD) has been found among alcoholics. However, little is known about the effect of VDD on alcoholic liver disease and the molecular mechanisms remain unclear. The aim of the current study was to evaluate whether vitamin D was deficient among patients with alcoholic fatty liver...

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Bibliographic Details
Published in:Free radical biology & medicine 2024-11, Vol.224, p.220-231
Main Authors: Wang, Huihui, Gong, Weiyi, Gao, Jingxin, Cheng, Wenxiu, Hu, Yongdi, Hu, Chunqiu
Format: Article
Language:English
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Summary:Vitamin D deficiency (VDD) has been found among alcoholics. However, little is known about the effect of VDD on alcoholic liver disease and the molecular mechanisms remain unclear. The aim of the current study was to evaluate whether vitamin D was deficient among patients with alcoholic fatty liver disease (AFLD) and the effect of VDD on chronic alcoholic liver injury and possible molecular mechanisms in mice. Our results found that lower 25-hydroxyvitamin D [25(OH)D] concentrations in patients with AFLD. And further analysis found that 25(OH)D is a protective factor in patients with AFLD. Mice experiments indicated that VDD can alter the composition of gut microbiota, down-regulate the protein levels of intestinal tight junction protein Occludin and E-cadherin, up-regulate the expression of inflammatory cytokines (tnf-α, il-1β, il-6, il-8, ccl2, il-10) in liver and colon tissue. And further exacerbated the protein levels of p65,P-IκB,P-p65 in alcoholic liver injury mice. In conclusion, VDD aggravates chronic alcoholic liver injury by activating NF-κB signaling pathway. [Display omitted] •Lower vitamin D levels in patients with alcoholic fatty liver disease(AFLD).•Vitamin D deficiency was able to up-regulate the expression of inflammatory cytokines by activating the NF-κB signaling pathway, alter the composition of gut microbiota and down-regulate the expression of tight-junction proteins.
ISSN:0891-5849
1873-4596
1873-4596
DOI:10.1016/j.freeradbiomed.2024.08.037