The Use of Sodium-Glucose Cotransporter 2 Inhibitors in Non-Alcoholic Fatty Liver Disease



 

Opinion

Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of progressive liver abnormalities from simple hepatic steatosis to non-alcoholic steatohepatitis (NASH) to advanced fibrosis, cirrhosis, and/or hepatocellular carcinoma [1]. Parallel to the rising burden of obesity and metabolic syndrome, NAFLD has emerged as the leading cause of chronic liver disease at an estimated global prevalence of 24% [2]. Besides its known clinical burden for liver-related morbidity and mortality, NAFLD is potentially linked with other extra-hepatic chronic diseases and may be considered a multisystem condition. Particularly, NAFLD increases the risk of type 2 diabetes, cardiovascular diseases, chronic kidney disease, and all-cause mortality [1]. Potential pathophysiologic mechanisms underlying the detrimental effects of NAFLD include hyperglycemia, systemic inflammation, and increased oxidative stress [3]. Sodiumglucose cotransporter 2 (SGLT2) inhibitors are a new class of antidiabetic agents that inhibit the reabsorption of sodium and glucose in the proximal tubules of the kidney [4]. Commonly used SGLT2 inhibitors include canagliflozin, dapagliflozin, and empagliflozin. Large-scale randomized placebo-controlled trials have demonstrated the benefits of SGLT2 inhibitors in reducing adverse cardiovascular/renal events in patients with cardiometabolic conditions, including diabetes, obesity, and chronic kidney disease [5]. In regard to liver function, numerous studies have revealed that SGLT2 inhibition reduced the levels of partate aminotransferase (AST) as well as alanine aminotransferase (ALT) in patients with type 2 diabetes and established cardiovascular disease [6], highlighting the potential role of SGLT2 inhibitors in patients with NAFLD.

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