S.Y. Pan 1 , Z.L. Yu 2 1 Beijing University of Chinese Medicine, 2 Hong Kong Baptist University Effects of the ethanolic extract of Fructus Schisandrae Chinensis (EtFSC) on serum and liver lipid contents were investigated in mice fed with normal diet or high fat/cholesterol diet for 8 or 15 days. Single dose of EtFSC (1 or 5 g/kg/day, i.g.) increased the serum triglyceride (TG) level (40 and 142%, respectively), but decreased hepatic total cholesterol (TC) level (15 and 16%, respectively) in normal mice. The hypertriglyceridemia produced by EtFSC was suppressed by the co-administration of fenofibrate. The induction of hypercholesterolemia by high fat/cholesterol diet caused significant increases in serum and hepatic TC levels (up to 165%) and hepatic TG levels (up to 528%) in mice. EtFSC treatment (1 or 5 g/kg/day for 7 days, i.g.) significantly decreased the mouse hepatic TG level (by 35%) and slightly increased the hepatic index (by 8%). Whereas fenofibrate treatment (0.1 g/kg/day for 7 days, i.g.) significantly lowered the hepatic TG level (by 61%), it significantly elevated the hepatic index (by 77%) in hypercholesterolemic mice. The results indicate that EtFSC treatment can invariably decrease hepatic TG in hypercholesterolemic mice, suggesting its potential use for fatty liver treatment. Aim: To investigate the influence of multiple gene polymorphisms in the susceptibility of NAFLD. Methods: The data of single nucleotide polymorphisms (SNPs) in 201 NAFLD patients who had at least one of the genetic variations at the sites of TNF--238, adiponectin -45 and leptin-2548 were analyzed. The genotypes were determined by using PCR-RFLP. Our previous studies showed that the variations of these sites increased the susceptibility of NAFLD. Results: The prevalence of NAFLD in adiponectin variation alone group (n=45) was 35.6%; in TNF-alone group (n=33) 42.4%; in leptin alone group (n=54) 35.2% (p>0.05). In comparison with the above groups with single SNP, the prevalence of the groups with two gene variations of TNF-plus adiponectin (57.9%, n=19) increased significantly (p<0.05). However the prevalence of other two groups i.e. adiponectin plus leptin (34.6%, n=26) and TNF-plus leptin (40.0%, n=15) did not differed significantly from those of groups with single SNP (p>0.05). The prevalence in the group with three gene variations (55.6%) differed significantly from all (p<0.05) except that of TNF-plus adiponectin group (p>0.05). The metabolic features of the NAFLD patients in the 7 groups mentioned above were not different significantly (p>0.05). Conclusion: NAFLD is a polygenic disease. Multiple gene polymorphisms may, but not always, increase the susceptibility of NAFLD.