In general, fructose reduces adipose tissue lipolysis [105], increases FA clearance, increases VLDL remnant concentrations [106] and promotes a shift to energy sourcing by promoting carbohydrate oxidation through complex pathways [107], which ultimately leads to both fasting and postprandial hypertriglyceridemia and non-alcoholic fatty liver disease (NAFLD), effects that are amplified in a hyperinsulinemic, insulin-resistant environment. This evidence concerns the gene INS and hypertriglyceridemia.