When the subgroup analyses were carried out
according to gender, BAY 73-4506 nmr both the genotypes and allelic frequencies in the female NAFLD group were significantly different from those in controls (P < 0.05), while there was no significant difference between the two male groups (P > 0.05). These results suggested that the G/A variant at leptin gene -2548 is associated with increased susceptibility to NAFLD in women. The genotypic distributions and allelic frequencies of the PPAR-γ gene -161 C/T polymorphism in the NAFLD group were significantly different from those in the control group (P < 0.05), but the difference was not significant in the PGC-1α gene -482 G/S polymorphism (P > 0.05). Our findings suggested that the C/T variant in the PPAR-γ gene increased susceptibility to NAFLD, and that the G/S variant in the PGC-1α genes was not relevant. Gender analyses showed no significant difference. The genotypic distributions and allelic frequencies at promoter region -514 C/T of the hepatic lipase gene were significantly different across groups (P < 0.05), suggesting that the C/T variant in the hepatic lipase learn more gene decreased susceptibility to NAFLD. The subgroup analysis according to gender showed no significant difference. The genotypic distributions and allelic frequencies at 175 G/A in exon 8 of the PEMT gene were significantly different between the NAFLD and control groups (P < 0.05). The
results pointed to a relationship between the G/A variant in
the PEMT gene and susceptibility to NAFLD. Gender analysis showed no significant difference. Genetic influences on susceptibility to metabolic syndrome have been reported, but the conclusions are controversial, and the associations are unclear.7–9 As an example, a meta-analysis including 31 observational studies found conclusions in most reports that the TNF-α -308 G/A variant was not involved in the pathogenesis of metabolic syndrome.18 However, other studies show an association between this variant and metabolic syndrome.19 There is less disagreement about the adiponectin gene; almost all papers supported an association with metabolic syndrome occurrence.20–23 As NAFLD represents the hepatic manifestation of metabolic syndrome, there is substantial overlap in the pathogenesis Fossariinae of these two syndromes.10–12 Theoretically, many variations in candidate genes contribute to the pathogenesis of NAFLD: first, genes related to insulin resistance, such as adiponectin, resistin, insulin receptor, PPAR-γ, etc.; second, genes impacting hepatic lipid metabolism, such as hepatic lipase, leptin (or leptin receptor), adiponectin, microsomal triglyceride transfer protein (MTP), PEMT, PPAR-α, cytochrome P450 (CYP) 2E1 and 4A, etc.; third, cytokine-related genes, such as TNF-α, interleukin (IL)-10, etc.; fourth, genes impacting liver fibrosis, such as leptin, adiponectin, transforming growth factor β1 (TGF-β1), connective tissue growth factor (CTGF), angiotensinogen, etc.