Methods:

A total of 101 obese children aged 6–17 years were recruited. 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 among 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 two classes: class S included shorter (27) repeats, and class L included longer (⩾ 27) repeats. We assessed the effects of the length of (GT) n repeats in HO-1 gene promoter on pediatric NAFLD.

Results:

Of the 101 obese subjects, 27 (26.7%) had NAFLD. The alanine aminotransferase 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|− 1 versus 30.2±20.1 IU|− 1; P= 0.027). The significant risk factors for pediatric NAFLD were patients carrying L alleles (L/L and L/S)(odds ratio (OR)= 18.84; 95% confidence interval (CI): 1.45–245.22; P= 0.025), homeostasis model assessment of insulin resistance (OR= 1.40; 95% CI: 1.07–1.83; P= 0.014) and age (OR= 1.24; 95% CI: 1.03–1.50; P= 0.025).

Conclusion:

In this hospital-based study, the obese children with longer GT repeats in the HO-1 gene promoter and insulin resistance were susceptible to NAFLD.