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中国儿童中β细胞功能和胰岛素抵抗与儿童2型糖尿病的关联。

Association of β-cell function and insulin resistance with pediatric type 2 diabetes among Chinese children.

作者信息

Xu Zhen-Ran, Du Hong-Wei, Cui Lan-Wei, Zheng Rong-Xiu, Li Gui-Mei, Wei Hai-Yan, Lu Fei-Yu, Chen Li-Li, Wu Chu-Shan, Zhang Shu-Xin, Zhang Shu-Le, Liu Fang, Zhang Miao-Ying, Pei Zhou, Sun Cheng-Jun, Wu Jing, Luo Fei-Hong

机构信息

Department of Pediatric Endocrinology and Inherited Metabolic Diseases, National Children's Medical Center, Children's Hospital of Fudan University, Shanghai 201102, China.

Department of Pediatric Endocrinology and Inherited Metabolic Diseases, The First Bethune Hospital of Jilin University, Changchun 130021, Jilin Province, China.

出版信息

World J Diabetes. 2021 Aug 15;12(8):1292-1303. doi: 10.4239/wjd.v12.i8.1292.

DOI:10.4239/wjd.v12.i8.1292
PMID:34512894
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8394231/
Abstract

BACKGROUND

In addition to insulin resistance, impaired insulin secretion has recently been identified as a crucial factor in the pathogenesis of type 2 diabetes mellitus (T2DM). Scarce clinical data exist for pediatric T2DM.

AIM

To investigate the association of β-cell function and insulin resistance with pediatric T2DM in the first Chinese multicenter study.

METHODS

This multicenter cross-sectional study included 161 newly diagnosed T2DM children and adolescents between January 2017 and October 2019. Children with normal glycemic levels ( = 1935) were included as healthy control subjects. The homeostasis models (HOMAs) were used to assess the β-cell function (HOMA2-%B) and insulin resistance (HOMA2-IR) levels. The HOMA index was standardized by sex and age. We performed logistic regression analysis to obtain odds ratios (ORs) for T2DM risk using the standardized HOMA index, adjusted for confounding factors including sex, Tanner stage, T2DM family history, body mass index z-score, and lipid profile.

RESULTS

The male-female ratio of newly diagnosed T2DM patients was 1.37:1 (OR = 2.20, = 0.011), and the mean ages of onset for boys and girls were 12.5 ± 1.9 years and 12.3 ± 1.7 years, respectively. The prevalence of related comorbidities including obesity, elevated blood pressure, and dyslipidemia was 58.2%, 53.2%, and 80.0%, respectively. The T2DM group had lower HOMA2-%B levels ( < 0.001) and higher HOMA2-IR levels ( < 0.001) than the control group. Both the decrease in HOMA2-%B z-score (OR = 8.40, 95%CI: 6.40-11.02, < 0.001) and the increase in HOMA2-IR z-score (OR = 1.79, 95%CI: 1.60-2.02, < 0.001) were associated with a higher risk of T2DM, and the decrease in HOMA2-%B z-score always had higher ORs than the increase in HOMA2-IR z-score after adjusting for confounding factors.

CONCLUSION

Besides insulin resistance, β-cell function impairment is also strongly associated with Chinese pediatric T2DM. Gender difference in susceptibility and high comorbidities warrant specific T2DM screening and prevention strategies in Chinese children.

摘要

背景

除胰岛素抵抗外,胰岛素分泌受损最近被确定为2型糖尿病(T2DM)发病机制中的一个关键因素。关于儿童T2DM的临床数据稀缺。

目的

在首个中国多中心研究中,探讨β细胞功能和胰岛素抵抗与儿童T2DM的关联。

方法

这项多中心横断面研究纳入了2017年1月至2019年10月期间161例新诊断的T2DM儿童和青少年。血糖水平正常的儿童(n = 1935)被纳入作为健康对照受试者。采用稳态模型(HOMAs)评估β细胞功能(HOMA2-%B)和胰岛素抵抗(HOMA2-IR)水平。HOMA指数按性别和年龄进行标准化。我们进行逻辑回归分析,以使用标准化的HOMA指数获得T2DM风险的比值比(ORs),并对包括性别、坦纳分期、T2DM家族史、体重指数z评分和血脂谱等混杂因素进行校正。

结果

新诊断的T2DM患者男女比例为1.37:1(OR = 2.20,P = 0.011),男孩和女孩的平均发病年龄分别为12.5±1.9岁和12.3±1.7岁。包括肥胖、血压升高和血脂异常在内的相关合并症患病率分别为58.2%、53.2%和80.0%。T2DM组的HOMA2-%B水平低于对照组(P < 0.001),HOMA2-IR水平高于对照组(P < 0.001)。HOMA2-%B z评分的降低(OR = 8.40,95%CI:6.40 - 11.02,P < 0.001)和HOMA2-IR z评分的升高(OR = 1.79,95%CI:1.60 - 2.02,P < 0.001)均与T2DM风险较高相关,在对混杂因素进行校正后,HOMA2-%B z评分的降低始终比HOMA2-IR z评分的升高具有更高的OR值。

结论

除胰岛素抵抗外,β细胞功能损害也与中国儿童T2DM密切相关。易感性的性别差异和高合并症需要在中国儿童中采取特定的T2DM筛查和预防策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5e/8394231/b52a9893ee97/WJD-12-1292-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5e/8394231/caabc1e02c2f/WJD-12-1292-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5e/8394231/b4c0f6f92ba5/WJD-12-1292-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5e/8394231/927917ad51f2/WJD-12-1292-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5e/8394231/b52a9893ee97/WJD-12-1292-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5e/8394231/caabc1e02c2f/WJD-12-1292-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5e/8394231/b4c0f6f92ba5/WJD-12-1292-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5e/8394231/927917ad51f2/WJD-12-1292-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b5e/8394231/b52a9893ee97/WJD-12-1292-g004.jpg

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