Natural Antioxidants for Non-alcoholic Fatty Liver Disease

Molecular Targets and Clinical Perspectives

Federico Salomone; Justyna Godos; Shira Zelber-Sagi


Liver International. 2016;36(1):5-20. 

In This Article

Coffee Polyphenols

Coffee is the most consumed beverage worldwide and its intake is associated with reduced all-cause mortality.[64] Several epidemiological studies have reported the association between coffee drinking and better metabolic status.[65,66] Studies with prospective cohorts have reported an inverse association between coffee consumption and liver cirrhosis and cancer, independently of aetiology.[67,68] Recently, cross-sectional studies have reported an inverse association between coffee consumption and liver fibrosis in the general population.[69–71] Part of the beneficial effects of coffee on liver health can be attributed to caffeine content at the molecular level.[72,73] Nonetheless, a recent study evaluating the effects of decaffeinated coffee intake on liver diseases has described an inverse association with serum levels of liver enzymes,[74] thus suggesting that the beneficial effects of coffee on liver health may be also dependent from other coffee components.[75] Vitaglione et al. has reported that consumption of coffee polyphenols in rats fed high fat diet exerted the same beneficial effects on liver injury of whole coffee intake; in particular, coffee polyphenols intake recapitulated the effects of whole coffee in decreasing oxidative, insulin resistance and fibrosis.[76] A further study of the effects of coffee polyphenols in rats with diet-induced obesity revealed that the polyphenolic fraction increases the expression of cell chaperones such as GRP-78, which is involved in correct protein folding and DJ-1 which regulates autophagy.[77,78] Interestingly, Pietrocola et al. extended these findings evidencing that coffee polyphenols stimulate autophagic flux in liver, muscle and heart. Recently, it was demonstrated that chlorogenic acid, a main coffee polyphenol, inhibits hepatic stellate cells activation in vitro,[79] thus providing a solid molecular rationale for the use of these compounds as antifibrogenic drugs in the clinical setting.