Figure 2.

Development of hepatic steatosis and its association with metabolic syndrome (MS). Part 1: Overweight/obesity leads extra-hepatic tissues to insulin resistance (IR), resulting in hyperglycemia and increased influx of FFA into the blood, common factors in the development of key components of MS (hypertension, obesity/dyslipidemia, diabetes mellitus (DM)), similar to NAFLD. NAFLD also increases glucose levels and release of FFA in the blood, contributing to the maintenance of IR; Part 2: Input-excess dietary glucose/fructose and hyperglycemia, increased lipid synthesis via DNL and increased dietary fat and adipose tissue lipolysis exacerbating IR, increased lipogenesis. Output corresponds to oxidative mitochondrial dysfunction and production of VLDL. Hepatic steatosis in both processes is impaired in function. NAFLD: nonalcoholic fatty liver disease; Input: synthesis and esterification of fatty acids; FFA: free fatty acids; DNL: de novo lipogenesis; Output: fatty acid oxidation and hepatic triglycerides exportation; VLDL: very low density lipoproteins.