Nonalcoholic fatty liver disease (NAFLD) results from fat accumulation within the liver and ranges from simple steatosis to steatohepatitis progressing to cirrhosis. NAFLD has become the most common cause of liver disease in the United States and Europe because of an aging population and increased prevalence of metabolic syndrome characterized by hypertension, hyperlipidemia, type 2 diabetes (T2DM), and central obesity.1 NAFLD is strongly associated with obesity and T2DM, where the prevalence of NAFLD in patients undergoing bariatric surgery exceeds 90% compared with an estimated prevalence of 25% in the general population.2 In patients with NAFLD, the estimated prevalence rates of obesity and T2DM are estimated at 51.3% and 22.5%, respectively, compared with 39.8% and 14.0% in the general US population.2 Currently, there are no US Food and Drug Administration (FDA)-approved interventions to treat NAFLD; therefore, lifestyle modifications and weight loss are the mainstay of therapy, where 3%–5% total body weight loss improves steatosis and 7%–10% can improve fibrosis.
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