Dyslipidemia is one of the hallmarks of the metabolic syndrome and has been shown to be strongly associated with NAFLD . Dyslipidemia associated with NAFLD is typically characterized by elevated levels of circulating TG and low-density-lipoprotein cholesterol (LDL-C), as well as decreased HDL-C levels . Only rats fed HFr-diet developed dyslipidemia, as defined by the presence of hypertriglyceridemia. Previous studies have also found that dietary fructose potently increase TG in plasma within a relatively short timeframe in both rats and mice [34, 38]. In rats, this has been suggested to be caused in part by the ability of fructose to both increase hepatic very-low-density-lipoprotein (VLDL)-TG secretion and decrease VLDL-TG clearance from the circulation, even in the absence of hyperinsulinemia [39, 40]. Mechanistically, the increase in VLDL-TG secretion has been proposed to result from a combined effect of fructose-induced hepatic stress responses , and activation of hepatic enzymes involved in the de novo synthesis of fatty acids (de novo lipogenesis) .