Key result
Recombinant resistin induced the occurrence and development of NAFLD and hepatic fibrosis by increasing proinflammatory cytokines TNF-α and TGF-β1 compared with the control group.
Why the study?
Does resistin induce hepatic fibrosis in models of non-alcoholic fatty liver disease?
Does resistin induce hepatic fibrosis in models of non-alcoholic fatty liver disease?
Resistin may promote the development of hepatic fibrosis in non-alcoholic fatty liver disease through the induction of proinflammatory cytokines TNF-α and TGF-β1.
Animal data link resistin to NAFLD fibrosis via cytokines; leaves open human relevance and requires prospective validation.
To investigate the effects and possible mechanisms of resistin on hepatic fibrosis in non-alcoholic fatty liver disease, this review used an in vivo model utilizing Wistar rats with a high fat diet. Recombinant resistin was selected to play role in hepatic stellate cells in the HSC-T6 cell line. We observed the degrees of hepatic fibrosis, measured the levels of Liver fibrosis spectrum and detected expression levels of resistin mRNA and protein in liver tissue as well as the expression levels of TGFβ-1 and TNF-α mRNA in HSC-T6. The results showed that expression of resistin in rat liver tissue and the degree of hepatic fibrosis increased over time with a high fat diet. Along with the increased concentration of resistin and levels of fibrosis index, TGFβ-1and TNF-α also increased in HSC-T6 cells. Compared with the control group, significant differences were found between each group, suggesting resistin by proinflammatory cytokine TNF-α and TGF-β1 induced the occurrence and development of NAFLD in hepatic fibrosis.
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Yang et al. (2013) studied Non-alcoholic fatty liver disease (NAFLD). Recombinant resistin and high fat diet vs. Control group was evaluated on Degree of hepatic fibrosis and expression levels of resistin, TGFβ-1, and TNF-α. Recombinant resistin induced the occurrence and development of NAFLD and hepatic fibrosis by increasing proinflammatory cytokines TNF-α and TGF-β1 compared with the control group.
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