Abstract
To investigate the role of E23K polymorphism of the KCNJ11 gene on early onset of type 2 diabetes in school-aged children/adolescents in Taiwan, we recruited 38 subjects with type 2 diabetes (ages 18.6 ± 6.6 years; body mass index percentiles 83.3 ± 15.4) and 69 normal controls (ages 17.3 ± 3.8 years; body mass index percentiles 56.7 ± 29.0) from a national surveillance for childhood/adolescent diabetes in Taiwan. We searched for the E23K polymorphism of the KCNJ11 gene. We found that type 2 diabetic subjects had higher carrier rate of E23K polymorphism of KCNJ11 gene than control subjects (P = 0.044). After adjusting for age, gender, body mass index percentiles, and fasting plasma insulin, the E23K polymorphism contributed to an increased risk for type 2 diabetes (P = 0.047). K23-allele-containing genotypes conferring increased plasma insulin level during OGTT in normal subjects. However, the diabetic subjects with the K23-allele-containing genotypes had lower fasting plasma insulin levels after adjustment of age and BMI percentiles. In conclusion, the E23K variant of the KCNJ11 gene conferred higher susceptibility to type 2 diabetes in children/adolescents. Furthermore, in normal glucose-tolerant children/adolescents, K23 allele carriers had a higher insulin response to oral glucose loading.
Highlights
Diabetes mellitus in children and adolescents has long been considered primarily type 1 diabetes
We demonstrated that the E23K polymorphism of KCNJ11 gene increased susceptibility to type 2 diabetes (T2D) in childhood and adolescence
After Body mass index (BMI) is calculated for children and teens, the BMI number is plotted on the Centers for Disease Control and Prevention (CDC) BMI-for-age growth charts to obtain a percentile ranking
Summary
Diabetes mellitus in children and adolescents has long been considered primarily type 1 diabetes. Type 2 diabetes (T2D) is generally considered to be a disease of adults, the past 15–20 years have seen a dramatic increase in the prevalence of T2D in children and adolescents [1,2,3,4,5,6,7,8,9]. The pancreatic islet ATP-sensitive potassium channel complex (KATP) plays a major role in glucose-stimulated insulin secretion, serving as a strong candidate for T2D. The estimated β-cell function based on the HOMA-B was calculated based on the following formula: %B = 20 × fasting plasma insulin (FPI, μU/mL)/(fasting plasma glucose (FPG, mM) − 3.5) [33]. The substitution of G with A eliminated the BanII site
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