The investigators hypothesize that obesity gene variants can predict the efficacy of weight loss intervention in obese children. The aim of the study was to establish a polygenic risk score model to assess differences to assess differences in weight loss treatment outcomes. The investigators will also analyze whether these gene variants have an effect on obesity comorbidities (hypertension, hyperlipidemia, non-alcoholic fatty liver disease, type 2 diabetes, obstructive sleep apnea, polycystic ovary syndrome, etc.). For participants with non-simple obesity, the investigators will collect their complete family history, and perform whole exome sequencing to identify possible rare disease-causing genes.~The experimental design is as follows:~Obese children and adolescent subjects will undergo a 6-month weight loss intervention program and be followed for 12-18 months. The investigators will analyze obesity and fatty liver-related genes in these adolescents using next-generation gene sequencing and/or gene chips, perform polygenic risk score analysis, and use an additive model to total the number of variant loci weighted by effect size. Whole exome gene sequencing refers to the human DNA map (hg19), and Sanger sequencing will be used to confirm the correctness of the variant site.
Children with obesity are prone to suffering from metabolic diseases, which undoubtedly increases the burden of public health. Since obesity is a multiple gene disease, a comprehensive approach using polygenic risk scores (PRS), rather than individual genetic variant, may be a more appropriate method. The aim of the study was to establish a polygenic risk score model to assess differences to assess differences in weight loss treatment outcomes.