Non-alcoholic fatty liver disease: need for a balanced nutritional source

Abstract

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.

Protective effect of ursodeoxycholic acid, resveratrol, andN-acetylcysteine on nonalcoholic fatty liver disease in rats

“…Although fatty liver was proven to be induced efficiently by feeding experimental animals with high fat diet, we applied here a somewhat novel and attractive model based on deficiency of the essential components methionine and choline in diet, which was also applied by other authors (Ding et al, 2015;Jha et al, 2014). This model is also relevant to human NAFLD as it was proven recently that a complex interplay among methionine, choline, and other factors is essential for proper lipid metabolism in the liver, and that deficiency of methionine or choline in human diet is a leading factor to fatty liver progression (Tarantino, 2014;Veena et al, 2014).…”

Non-alcoholic fatty liver and the gut microbiota

“…High-fructose diet induces steatosis, along with other metabolic abnormalities associated with this diet, such as weight gain, insulin resistance, and hyperlipidemia [9]. Genetic NAFLD models include mutations associated with NAFLD predisposition, such as the ones noted in the PNPLA3 gene [10]. It is worth noting that there are phenotypic differences between PNPLA3 associated mouse models (deletion, induced expression/insertion, and transgenic) highlighting a potential caveat of using genetic models to delineate mechanisms involved in human disease [11].…”

Extrahepatic Diseases and NAFLD: The Triangular Relationship between NAFLD, Type 2-Diabetes and Dysbiosis

“…NAFLD has a multifactorial pathophysiology involving genetic (PNPLA3 I148M polymorphism) [4] and metabolic factors, such as sedentary lifestyle, increased intake of energy-rich foods, malnutrition characterized by an imbalanced intake of nutrients (e.g., high fat and high proteins diet, low fiber intake, high fructose intake) [5] , altered gut microbiota composition (dysbiosis) [6] , obesity, insulin resistance and T2DM [7] . The interaction between diet, host and gut microbiota can modulate inflammatory signaling pathways that in turn cause obesity, NAFLD and insulin resistance.…”