Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are an increasingly common chronic liver disease closely associated with diabetes and obesity that have reached epidemic proportions. Reports on the prevalence of NAFLD have suggested that 27-34 % of the general population in the USA and 40-90 % of the obese population worldwide have this disease. Increasing urbanisation rate and associated inappropriate lifestyle changes are not only the risk factors of diabetes, but also unmask genetic predisposition in various populations for the metabolic syndrome and its manifestations including NAFLD and NASH. Lifestyle modifications and balanced nutrition are among the foremost management strategies along with ursodeoxycholic acid, metformin, vitamin E and pentoxifylline. Although weight reduction associated with current therapeutic strategies has shown some promise, maintaining it in the long run is largely unsuccessful. With the safety of pharmacotherapy still being uncertain and can be started only after confirmation, other reasonable interventions such as nutrition hold promise in preventing disease progression. The role of dietary components including branchedchain amino acids, methionine, choline and folic acid is currently being evaluated in various clinical trials. Nutritional approaches sought to overcome the limitations of pharmacotherapy also include evaluating the effects of natural ingredients, such as silymarin and spirulina, on liver disease. Understanding the specific interaction between nutrients and dietary needs in NAFLD and maintaining this balance through either a diet or a nutritional product thus becomes extremely important in providing a more realistic and feasible alternative to treat NAFLD. A planned complete nutritional combination addressing specific needs and helping to prevent the progression of NAFLD is the need of the hour to avert people from ending up with complications.

ing significant reduction in certain long-(hexadecanoic and heptadecanoic), medium (hexanoic and octanoic), and short (butanoic) free fatty acids. Remarkably, the levels of octanoic acid (known to have antimicrobial properties) were dramatically reduced (~48 fold) in mice fed USF+EtOH compared to SF+EtOH fed animals. A decline in certain fecal amino acids (e.g. serine and glycine) was observed in USF+EtOH fed animals. Conclusions: These data support an important role of dietary lipids in ALD pathogenesis, and provide insight into mechanisms of ALD development. A diet enriched in USF not only enhanced alcohol-induced liver injury, but also caused major fecal metagenomic and metabolomic changes that may play an etiologic role in observed liver injury. Characterization of both microbiota composition and function is an important approach to investigate host-microbial interaction. Our data suggest that dietary lipids can potentially serve as interventions for the prevention/treatment of ALD.