Conclusions and Future Perspectives
Taken together, these studies provide reasonably strong evidence for a protective effect of coffee consumption on development of NAFLD, and on reducing its severity in NASH. Since the most convincing effect of coffee consumption on other forms of liver disease is its association with a substantially reduced rate of HCC, future studies on HCC in NAFLD examining coffee consumption with other potential environmental factors (fructose, vegetables, smoking, vitamin D, and selenium, etc.) are keenly awaited. Meanwhile, it does appear that possible hepatoprotective effects of coffee are related more to polyphenols not caffeine. The possible protective effects of coffee bean polyphenols may be related to a diverse range of mechanisms, including anti-oxidant, anti-inflammatory, anti-fibrotic pathways as well as modulation in energy metabolism, reduced insulin resistance, and reduced severity of diabetes (Fig. 2). However, studies to date have been exploratory and confined to a limited range of experimental systems, only a small subset of which have utilized clinically relevant experimental models of NASH. It is clear that some components of coffee other than caffeine may be involved, and specific identification of these compounds require more rigorous study to elucidate the mechanisms underlying coffee's hepatoprotective effects in patients with NAFLD.
Schematic diagram illustrating the mechanisms underlying coffee's potential hepatoprotective effects in non-alcoholic fatty liver disease. CTGF, connective tissue growth factor; GSSG, oxidized glutathione; IFN-γ, interferon-γ; IL-10, interleukin-10; IL-1β, interleukin-1β; IL-4, interleukin-4; MCP-1, monocyte chemoattractant protein-1; NASH, non-alcoholic steatohepatitis; PPAR-α, peroxisome proliferator-activated receptor α; ROS, reactive oxygen species; Smad2, Mothers against decapentaplegic homolog 2, SMAD family member 2; SREBP-1C, sterol regulatory element-binding protein-1C; TGF-β, transforming growth factor β; TNF-α, tumor necrosis factor α.
J Gastroenterol Hepatol. 2014;29(3):435-441. © 2014 Blackwell Publishing