YI-DER JIANGLEE-MING CHUANGPei, DeeDeePeiLee, Yann-JinnYann-JinnLeeWei, Jun-NanJun-NanWeiSung, Fung-ChangFung-ChangSungTIEN-JYUN CHANG2023-02-082023-02-0820141687-8337https://scholars.lib.ntu.edu.tw/handle/123456789/627700To 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.enGENOME-WIDE ASSOCIATION; HOMEOSTASIS MODEL ASSESSMENT; BETA-CELL; CLINICAL CHARACTERISTICS; E23K POLYMORPHISM; YOUTH PREVALENCE; K+ CHANNEL; SUR1 ABCC8; MELLITUS; SEARCH[SDGs]SDG3journal article10.1155/2014/983016253095952-s2.0-84911893554WOS:000344689800001https://api.elsevier.com/content/abstract/scopus_id/84911893554