Other PLA2 isozymes might be involved in the generation of PGs responsible for regulating the expression of adiponectin. Alternatively, a deficiency of IVA-PLA2 might result in decreases in the levels of both inhibitory and stimulatory PGs on the production of adiponectin. Meanwhile, the serum levels of leptin correlate positively with adipose accumulation. Consistent with this, we show here that HF diets increased the serum levels of leptin with adipose accumulation in wild-type and IVA-PLA2-knockout mice. However, a deficiency of IVA-PLA2 did not affect the HF diet-induced increase in serum leptin levels. Considering the beneficial Sulfabenzamide effects of leptin on fatty liver, the changes in serum leptin levels under the HF dietary conditions Olprinone probably do not explain the reduced fatty liver damage in IVA-PLA2-knockout mice. Previous studies showed that the expression of leptin is inhibited by PGD2, PGJ2, and 15deoxy-PGJ2 in 3T3-L1 adipocytes, but stimulated by PGE2 in mouse adipose tissues in primary culture. As in the case of adiponectin mentioned above, the possible involvement of IVAPLA2 in the generation of PGs that regulate the production of leptin is unclear at present. To further clarify the role of IVA-PLA2 in the expression of adiponectin and leptin in adipocytes and colocalized inflammatory cells, experiments with preadipocytes and macrophages derived from IVA-PLA2-knockout mice are underway in our laboratory. Resistin has been implicated in the pathogenesis of obesitymediated insulin resistance. Increased serum levels of resistin are related to the histological severity of NAFLD in human subjects. A previous study demonstrated that hepatic TG content tended to be lower in resistin-deficient mice. These findings suggest that higher serum levels of resistin are a cause of the development of fatty liver. In the present study, no significant difference was observed in the serum levels of resistin in wild-type and IVA-PLA2-knockout mice. This observation is consistent with the lack of changes in the serum levels of insulin and glucose in both genotypes under the HF dietary conditions.