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Concurrent Session: Management of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in children and adults

Friday, May 6, 2016
1:45pm - 3:00pm


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Management of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in children and adults

This session will review the pathophysiology of nonalcoholic steatohepatitis and its impact on the health of children as well as it's treatment and prevention

Management of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in children
Dr. Massimiliano Paganelli

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in children, with a prevalence of about 38% in obese children. Approximately 25% of children with NAFLD develop nonalcoholic steatohepatitis (NASH), the progressive form of the disease. Oversupply of free fatty acids to hepatocytes, and/or their insufficient disposal, lead to the formation of lipotoxic lipids that cause hepatocellular oxidative stress. The interplay between regenerative and inflammatory responses can then result in the activation of stellate cells and the development of fibrosis. Dietary sugars, and fructose in particular, play a central role in NAFLD pathogenesis through de novo lipogenesis. Sugar is an independent risk factor for NAFLD, irrespective of its caloric content. Specific genetic polymorphisms have been shown to increase the deleterious effects of dietary fat and carbohydrates on the liver. The microbiome and bacterial metabolites, the crosstalk between hepatocytes and adipocytes, and the innate immune system, have all been implicated in the pathogenesis of NAFLD. Liver fat content plays a central role in insulin sensitivity, and is associated with prediabetes and cardiovascular complications. Liver fat and fibrosis can now be accurately quantified by non-invasive techniques like Fast-MRI or FibroScan, or predicted by several scores and biomarkers. Current treatment strategies are mostly based on physical exercise and dietary modifications to reduce insulin resistance and achieve gradual weight reduction. Both metformin and vitamin E did not show a significant effect in children. Preliminary data on new drugs acting on the farnesoid X receptor (FXR) seem promising. Bariatric surgery proved effective and could play an important role in treating a subgroup of adolescents with NAFLD.

Dietary sugars and the risks of non-acloholic fatty liver disease: what was known and what are the research gaps?
Dr. Mei Chung

Non-alcoholic fatty liver disease (NAFLD), formerly called non-alcoholic steatohepatitis, is characterized by hepatic steatosis, abnormal triglycerides accumulation in liver cells. Its etiology, pathophysiology and pathogenesis are still poorly understood. Some have suggested that the increased intake of sweeteners over the past few decades, particularly of high fructose corn syrup (HFCS), may be contributing to the increased incidence of NAFLD. A systematic review and meta-analysis was commissioned to examine the effect of different levels and forms of dietary sugars on the incidence or prevalence of NAFLD and on indices of liver health in humans.

A total of 6 observational studies and 21 intervention studies met the pre-defined study eligibility criteria.  Based on indirect comparisons across study findings, we concluded that the apparent association between indexes of liver health (ie, liver fat, hepatic de novo lipogenesis, alanine aminotransferase, AST, and y-glutamyl transpeptase) and fructose or sucrose intake appear to be confounded by excessive energy intake. Overall, the available evidence is not sufficiently robust to draw conclusions regarding effects of fructose, HFCS, or sucrose consumption on NAFLD. Several important research gaps were identified by our systematic review and will be discussed in this presentation.

Dietary composition and non-alcoholic fatty liver disease in morbidly obese patients
Katherine Schwenger (Abstract Presentation)

Non-alcoholic fatty liver disease (NAFLD) affects 15-30% of the general population, with increased prevalence in obesity. Amounts and composition of dietary intake contribute to obesity and could be associated with NAFLD severity. In morbidly obese (MO), there is little information about the relationship between diet and NAFLD severity. The aim of this study was to investigate whether diet is associated with histological features of NAFLD in MO patients. This is a cross-sectional study of morbidly obese patients who were recruited prior to bariatric surgery. A 3-day food record, anthropometrics and a liver biopsy were collected and the relationship between liver histology and dietary nutrients were examined. We found correlation between nutrients, specifically dietary sodium and trans-fat and liver histology. In conclusion, there may be an association between dietary composition and NAFLD severity based on histology in MO patients that may require future studies.



Dr. Mei Chung

Assistant Professor at the Department of Public Health and Community Medicine, Tufts University School of Medicine

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