The Evaluation of the Genetic Variation Types of the Gene by Next-Generation Sequencing and Their Effects on Bilirubin Levels in Obese Children

Obesity is a major nutritional problem with an increasing prevalence among children and adolescents. The () gene encodes the UDP-glucuronosyl transferase enzyme, converting the toxic form of bilirubin to a soluble, nontoxic form. There are yet to be studies on the evaluation of the variant types detected by next-generation sequencing (NGS) and their effects on bilirubin levels in nonsyndromic obese children. Forty-five children with body mass index (BMI) >95 percentile (p) constituted the obesity group and fourteen healthy children with BMI <85p constituted the control group. Anthropometric, clinical features, and biochemical parameters were evaluated. Furthermore, the gene was sequenced by NGS. The obese patients had lower total, direct, and indirect bilirubin levels ( = 0.422, 0.026, and 0.568, respectively). In addition, obese patients had more genetic variations in the gene compared with the control group (62.2% and 50%, respectively). We found that children with variations had higher total direct and indirect bilirubin levels compared with those without variation ( = 0.016, 0.028, and 0.015, respectively). Children diagnosed with obesity in the first two years of their life had fewer genetic variations and lower total bilirubin levels ( = 0.000 and 0.013, respectively). It is assumed that bilirubin can be protective against many chronic diseases. Although bilirubin levels are found to be lower in obese children compared with the control group, some variations in the gene may be supported by raising bilirubin. We suggest that high bilirubin levels caused by those variations may be protective against obesity and its many negative effects.