PROTECTION against alcoholic liver disease may become possible thanks to new research surrounding the protein fibroblast growth factor 21 (FGF21). A recent study, conducted by a team of researchers at the Beth Israel Deaconess Medical Center (BIDMC), Boston, Massachusetts, USA and colleagues from the University of Pennsylvania, Philadelphia, Pennsylvania, USA, found that the concentration of the FGF21 protein in the blood was massively increased following alcohol consumption in both humans and mice. Additionally, those mice which were bred to be lacking FGF21, endured greater liver damage upon alcohol consumption compared to their wild-type counterparts.
It is well established that excessive alcohol consumption can induce severe liver damage. Research concerning treatment and reversal of this damage is fundamental, as the only current therapy option for serious cases is liver transplantation. The FGF21 protein has previously been found to possess protective properties against diet-related liver toxicities in mice. This study extended past research by testing the relationship between FGF21 and alcohol-induced liver disease, including humans in the study as well as mice.
In mice lacking FGF21, alcohol was cleared from the body as per usual. Interestingly, mice that were bred to overexpress FGF21 were less likely to consume alcohol than the wild-type mice, and wild-type mice given additional FGF21 preferred water to alcohol, suggesting the presence of FGF21 inhibits alcohol consumption, further contributing to the protection against liver disease.
The study researchers hope to perform additional studies to confirm these results, with co-senior author Prof Eleftheria Maratos-Flier, Division of Endocrinology, Diabetes and Metabolism, BIDMC and Harvard Medical School, Boston, Massachusetts, USA stating: “Because humans and mice have similar responses, mice may be a good model for studying this further.” Future research will assess the protective effects of FGF21 in mice in terms of limiting or reversing liver damage, as well as investigating the possibility of using the protein to inhibit alcohol consumption in humans.
Prof Maratos-Flier concluded: “Our results may encourage the development of drugs that mimic FGF21 for the treatment of alcoholic liver disease, and possibly to produce alcohol aversion.” This study, therefore, is highly exciting for the future of liver disease treatments, with the prospect of much needed, brand new, therapeutic drugs becoming a very real possibility.
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