In addition, the changes in the serum levels of phospholipids and lysophosphatidylcholine may be correlated with the serum levels of LDL. However, under our experimental conditions, wild-type mice on HF diets Nitisinone exhibited no change in the serum levels of not only FFA, adiponectin, and resistin, but also TG, glucose, or insulin, despite hepatic and adipose fat deposition. Thus, HF diet-fed wild-type mice developed fatty liver and adipose accumulation in the absence of significant features of metabolic disorders. This suggests that the HF diet-induced hepatic fat deposition is mediated in part by the direct deposition of dietary fats, as in the case of adipose tissues, in wild-type mice. Our recent and the present studies showed that hepatic TG content was lower in IVA-PLA2-knockout mice than in wild-type mice under Paroxetine HCl normal dietary conditions, suggesting a physiological role of IVA-PLA2 in the regulation of TG accumulation in the liver. Furthermore, HF diet-induced increase in hepatic TG content was partially suppressed in IVA-PLA2-knockout mice compared with wild-type mice, the reduced level being almost at the level observed in wild-type mice fed normal diets. It is, consequently, possible that since IVA-PLA2 is physiologically involved in the regulation of TG content in the liver, a lack of IVA-PLA2 somewhat prevents hepatic TG deposition even caused by excess dietary fat intake, thereby resulting in the alleviation of large hepatic vacuolation. It has been suggested that PGE2 plays a role in hepatocellular TG accumulation. In IVA-PLA2-knockout mice, serum PGE2 levels were indeed reduced. However, other IVA-PLA2 metabolites, such as other eicosanoids and lysophospholipids, are also probably reduced in IVA-PLA2-knockout mice. Therefore, IVA-PLA2 metabolites responsible for the accumulation of hepatic TG are unclear at present. Meanwhile, a recent study showed that an HF diet-induced increase in the mass of visceral adipose tissues precedes the development of fatty liver accompanied with no significant change in the serum levels of FFA, TG, or adiponectin in moderately obese mice.