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Non-alcoholic fatty liver disease is the hepatic manifestation of the global epidemic of metabolic disease. It is tightly associated with obesity and type 2 diabetes, yet the precise mechanisms that drive its aetiology are not fully defined. Steroid hormones, including glucocorticoids and sex steroids, regulate metabolic phenotype; additionally, bile acids have recently been identified as potent metabolic regulators. AKR1D1 (5β-reductase), is predominantly expressed in the liver, and is a crucial regulator of steroid hormone clearance as well as bile acid synthesis. Its role in pathogenesis of metabolic disease has not been examined. We therefore developed systems to define the enzymology of human AKR1D1 in cell free assays and to determine the impact of manipulation of AKR1D1 expression and activity in human hepatocyte models. Background

Model systems to define the role of AKR1D1 in metabolic liver disease