Childhood Weight, Stature, and Body Mass Index Among Never Overweight, Early-Onset Overweight, and Late-Onset Overweight Groups

PEDIATRICS ◽  
2000 ◽  
Vol 106 (1) ◽  
pp. e14-e14 ◽  
Author(s):  
Wayne Wisemandle ◽  
L. Michele Maynard ◽  
Shumei S. Guo ◽  
Roger M. Siervogel
2022 ◽  
Author(s):  
Yunyun Fang ◽  
Jingjing Zhang ◽  
Linlin Ji ◽  
Chaoyu Zhu ◽  
Yuanyuan Xiao ◽  
...  

Abstract Objective: To investigate the relationship between glucagon-like peptide-1 receptor (GLP1R) gene polymorphisms and susceptibility to early-onset type 2 diabetes (EOD).Methods: Samples from 316 type 2 diabetes (T2DM) patients with EOD (n = 137) and late-onset T2DM (n = 179) and 145 non-diabetic individuals were analyzed. Multiplex PCR combined with resequencing HI-Reseq technology was used to detect single nucleotide polymorphisms (SNPs) of the GLP1R gene, and the allele frequency, genotype distribution, and clinical parameters were analyzed between each diabetes subgroup and the control group.Results: Sixteen SNPs were identified in the exonic region of the GLP1R gene according to the minor allele frequency (MAF > 0.05) in the participants. Among these, the GLP1R rs3765467 (G→A) mutation was statistically associated with EOD. Compared with that of the GG carriers, carriers of genotype AA at rs3765467 had a decreased risk of EOD after adjusting for sex and body mass index. In the dominant model, the frequencies of the rs3765467 AA+GA genotype were significantly decreased in the EOD group, and carriers of genotype AA+GA at rs3765467 had a decreased risk of EOD after adjusting for sex and body mass index. Moreover, fasting c peptide levels were significantly higher in GA+AA genotype carriers than that in GG genotype carriers.Conclusion: The GLP1R rs3765467 polymorphism was significantly associated with the age at T2DM diagnosis, and thus may be used as a marker to screen and detect individuals at risk of developing EOD.The name of the clinical trials registry: Exploration of early warning indicators for diabetic chronic complications. The approval number is 2016-004.The approval date is June 12, 2016.


2016 ◽  
Vol 22 (9) ◽  
Author(s):  
Yanchang Zhang ◽  
Brenda Cartmel ◽  
Courtney C Choy ◽  
Annette M Molinaro ◽  
David J Leffell ◽  
...  

PLoS ONE ◽  
2017 ◽  
Vol 12 (4) ◽  
pp. e0175728 ◽  
Author(s):  
Arshad M. Channanath ◽  
Naser Elkum ◽  
Dalia Al-Abdulrazzaq ◽  
Jaakko Tuomilehto ◽  
Azza Shaltout ◽  
...  

2017 ◽  
Vol 46 ◽  
pp. 66-72 ◽  
Author(s):  
Yanchang Zhang ◽  
Brenda Cartmel ◽  
Courtney C. Choy ◽  
Annette M. Molinaro ◽  
David J. Leffell ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Yi-Der Jiang ◽  
Lee-Ming Chuang ◽  
Dee Pei ◽  
Yann-Jinn Lee ◽  
Jun-Nan Wei ◽  
...  

To investigate the role of E23K polymorphism of theKCNJ11gene 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 theKCNJ11gene. We found that type 2 diabetic subjects had higher carrier rate of E23K polymorphism ofKCNJ11gene 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 theKCNJ11gene 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.


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