Mutations of SNPs (rs2075596, rs2239464) of MeCP2 showed increased risk of developing SLE. Large-scale multicenter epidemiological studies in selected populations with other risk factors are urgently required.

Background and aims The pathogenesis of paediatric nonalcoholic fatty liver disease (NAFLD) has not been fully elucidated. This study aimed to assess the association of the length of (GT)n repeats in HO-1 gene promotor and insulin resistance with NAFLD among obese children. Methods A total of 101 obese children aged 6–17 years were recruited. The diagnosis of NAFLD was made by liver ultrasonography. Anthropometric, serum biochemical variables and biomarkers for glucose and insulin metabolism were measured. We screened the allelic frequencies of (GT)n repeats in the HO-1 gene promoter in these obese children. NAFLD was determined through liver ultrasonography. Because the distribution of numbers of (GT)n repeats was bimodal, we divided the alleles into 2 subclasses: class S included shorter (n repeats in HO-1 gene promoter on paediatric NAFLD. Results Of 101 obese subjects, 27 (26.7%) had NAFLD. The alanine aminotransferase (ALT) level was higher in patients carrying L alleles (L/L and L/S) than patients with S alleles (S/S) [46.2 ± 49.3 IU/L versus 30.2 ± 20.1 IU/L]. The significant risk factors for paediatric NAFLD were patients carrying L alleles (L/L and L/S) (11.613; 95% CI, 1.2 to 112.43; p = 0.034), and HOMAR-IR (1.37; 95% CI, 1.05 to 1.79; p = 0.019). Conclusions In this hospital-based study, the obese children with larger GT repeats and insulin resistance were susceptibility to have NAFLD.