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妊娠期糖尿病与2型糖尿病之间的关系:线粒体功能障碍的证据

Relationship between gestational diabetes mellitus and type 2 diabetes: evidence of mitochondrial dysfunction.

作者信息

Weijers Rob N M, Bekedam Dick J

机构信息

Department of Clinical Chemistry and Haematology, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands.

出版信息

Clin Chem. 2007 Mar;53(3):377-83. doi: 10.1373/clinchem.2006.077636.

DOI:10.1373/clinchem.2006.077636
PMID:17327503
Abstract

BACKGROUND

We examined the pathogenesis of gestational diabetes mellitus (GDM) in a large Dutch multiethnic cohort.

METHODS

We used a 2-step testing procedure to stratify 2031 consecutive pregnant women into 4 groups according to American Diabetes Association criteria: (a) normal glucose tolerance (NGT), (b) mild gestational hyperglycemia (MGH), (c) GDM without early postpartum diabetes within 6 months of delivery (GDM1), and (d) GDM with early postpartum diabetes (GDM2). Antepartum and postpartum clinical characteristics and measures of glucose tolerance were documented.

RESULTS

Overall, 1627 women had NGT, 237 had MGH, 156 had GDM1, and 11 had GDM2. Prepregnancy body mass index values progressively increased from NGT to MGH to GDM1. The fasting plasma glucose concentration, the 100-g oral glucose tolerance test (OGTT) area under the curve, and the mean glucose concentration during the OGTT all increased progressively among the 4 groups. The fasting C-peptide concentration displayed an inverted-U pattern, with a maximum at a mean plasma glucose concentration during the OGTT of 9.6 mmol/L in the transition from GDM1 to GDM2. The fasting C-peptide/glucose concentration ratio decreased by 42% in GDM patients compared with NGT patients, whereas the ratios in MGH and NGT women were similar.

CONCLUSIONS

Progressive metabolic derangement of glucose tolerance 1st detected during pregnancy mimics the pathogenesis of type 2 diabetes. In addition, our results imply an impaired basal glucose effectiveness in the early prediabetic state. To explain the parallel in both metabolic derangements, we postulate that GDM, like type 2 diabetes, is attributable to the same inherited mitochondrial dysfunction.

摘要

背景

我们在一个大型荷兰多民族队列中研究了妊娠期糖尿病(GDM)的发病机制。

方法

我们采用两步检测程序,根据美国糖尿病协会标准将2031名连续的孕妇分为4组:(a)正常糖耐量(NGT),(b)轻度妊娠高血糖(MGH),(c)分娩后6个月内无早期产后糖尿病的GDM(GDM1),以及(d)伴有早期产后糖尿病的GDM(GDM2)。记录产前和产后的临床特征以及糖耐量指标。

结果

总体而言,1627名女性为NGT,237名有MGH,156名有GDM1,11名有GDM2。孕前体重指数值从NGT到MGH再到GDM1逐渐升高。空腹血糖浓度、100克口服葡萄糖耐量试验(OGTT)曲线下面积以及OGTT期间的平均血糖浓度在这4组中均逐渐升高。空腹C肽浓度呈现倒U形模式,在从GDM1过渡到GDM2时,OGTT期间平均血糖浓度为9.6 mmol/L时达到最高值。与NGT患者相比,GDM患者的空腹C肽/血糖浓度比值下降了42%,而MGH和NGT女性的该比值相似。

结论

孕期首次检测到的糖耐量进行性代谢紊乱类似于2型糖尿病的发病机制。此外,我们的结果表明在糖尿病前期早期基础葡萄糖有效性受损。为了解释这两种代谢紊乱的相似之处,我们推测GDM与2型糖尿病一样,归因于相同的遗传性线粒体功能障碍。

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