Genetic-specific Effects of Fructose on Liver Lipogenesis
Last updated on July 2021Recruitment
- Recruitment Status
- Recruiting
- Estimated Enrollment
- Same as current
Summary
- Conditions
- NAFLD
- Non Alcoholic Fatty Liver Disease
- Type
- Interventional
- Phase
- Not Applicable
- Design
- Allocation: Non-RandomizedIntervention Model: Parallel AssignmentIntervention Model Description: Participants are assigned to high genetic risk score group in parallel to low genetic risk score groupMasking: None (Open Label)Primary Purpose: Basic Science
Participation Requirements
- Age
- Between 12 years and 40 years
- Gender
- Both males and females
Description
BACKGROUND AND RATIONALE Non-alcoholic fatty liver disease (NAFLD) is characterized by fat accumulation in liver cells not caused by alcohol. A leading cause of chronic liver disease in the US, NAFLD represents a group of disorders including steatosis, nonalcoholic steatohepatitis with fibrosis. It ...
BACKGROUND AND RATIONALE Non-alcoholic fatty liver disease (NAFLD) is characterized by fat accumulation in liver cells not caused by alcohol. A leading cause of chronic liver disease in the US, NAFLD represents a group of disorders including steatosis, nonalcoholic steatohepatitis with fibrosis. It has substantially risen in prevalence over the last two decades with the estimated prevalence being 20% among US adults and 25% in young adults (18-39 years). Over 64 million individuals are believed to have NAFLD with annual medical costs rising to more $100 billion. More common in individuals who are obese or diabetic and/or have metabolic syndrome, NAFLD has been associated with increased cirrhosis, liver-related mortality and hepatocellular carcinoma. Both genetic and environmental, including nutritional, factors contribute to the onset and progression of NAFLD. Increased consumption of sugar-sweetened, fructose-rich beverages has been linked to NAFLD. Fructose, commonly found in soft drinks, fruit juices and energy drinks, affects many metabolic processes, foremost being an increase in fat accumulation in the liver and hence, NAFLD. Genome-wide and candidate gene studies have identified several genes associated with NAFLD. However, none of these studies have shown the cumulative effects of single nucleotide polymorphisms (SNPs) on changes in liver fat when exposed to fructose. The results from this study can be extrapolated to larger cohorts and other ethnicities and are therefore, expected to lay the foundation for developing personalized nutritional plans.
Tracking Information
- NCT #
- NCT03783195
- Collaborators
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
- Investigators
- Principal Investigator: Saroja Voruganti University of North Carolina, Chapel Hill