Comments on: A functional polymorphism rs10830963 in melatonin receptor 1B associated with the risk of gestational diabetes mellitus.

评论: 褪黑激素受体1B的功能多态性rs10830963与妊娠糖尿病风险相关。

  • 影响因子:2.87
  • DOI:10.1042/BSR20194316
  • 作者列表:"Rosta K","Harreiter J","Nádasdi Á","Németh L","Kautzky-Willer A","Somogyi A","Firneisz G
  • 发表时间:2020-02-28

:We have read with great interest the accepted manuscript of the meta-analysis performed by Huang, et al. titled "A functional polymorphism rs10830963 in melatonin receptor 1B associated with the risk of gestational diabetes mellitus" published online in the 2019 December 6 issue of Bioscience Reports (https://doi.org/10.1042/BSR20190744). We do agree with the authors' final conclusion that such a meta-analysis should eventually confirm that the MTNR1B rs10830963 G allele is significantly associated with increased risk of gestational diabetes mellitus (GDM) development in pregnant populations with Asian and European ancestry. However we have surprisingly found that our genetic association study (PLoS One (2017), https://doi.org/10.1371/journal.pone.0169781) was included in this meta-analysis, but with mistakenly calculated odds ratios (OR). Therefore we would suggest to use the correct OR values based on our original publication that were already indicating a high genetic effect size for the MTNR1B rs10830963 risk variant on GDM development.


: 我们饶有兴趣地阅读了黄等人进行的荟萃分析的公认手稿,题为 “褪黑激素受体1B中的功能多态性rs10830963与妊娠糖尿病的风险相关”,在线发表在2019 12月6日的生物科学报告 ( https://doi.org/10.1042/BSR20190744 )。我们确实同意作者的最终结论,即这样的荟萃分析最终应该证实MTNR1B rs10830963 G等位基因与亚洲和欧洲血统的孕妇群发生妊娠期糖尿病 (GDM) 的风险增加显著相关。然而,我们惊奇地发现,我们的遗传关联研究 (PLoS One (2017), https://doi.org/10.1371/journal.pone.0169781 ) 被纳入该荟萃分析,但错误地计算了比值比 (OR)。因此,我们建议根据我们的原始出版物使用正确的OR值,这些值已经表明MTNR1B rs10830963风险变体对GDM发展的高遗传效应大小。



作者列表:["Landon MB","Mele L","Varner MW","Casey BM","Reddy UM","Wapner RJ","Rouse DJ","Tita ATN","Thorp JM","Chien EK","Saade G","Grobman W","Blackwell SC","VanDorsten JP","Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units (MFMU) Network."]

METHODS::Objective: To determine the association of maternal glycemia with childhood obesity and metabolic dysfunction.Study design: Secondary analysis of follow-up data 5-10 years after a mild gestational diabetes mellitus (GDM) treatment trial. The relationship between maternal oral glucose tolerance testing (OGTT) at 24-31-week gestation and body mass index (BMI), fasting glucose, insulin, and anthropometric measurements (sum of skinfolds, subscapular/triceps ratio, and waist circumference) in the offspring of untreated mild GDM and non-GDM (abnormal 50-g screen/normal OGTT) women was assessed. Multivariable regression modeling controlling for maternal and neonatal characteristics was employed.Results: A cohort of 236 untreated mild GDM and 480 non-GDM offspring were analyzed. In the combined cohort, significant correlations existed between fasting, 1, 2, and 3 h maternal glucose and subscapular/triceps ratio (all p < .04) and in all OGTT values other than the 2-hour value for homeostatic model assessment-estimated insulin resistance (HOMA-IR) (all p < .04) and sum of skinfold measurements (all p < .03). No correlation was found between OGTT values and childhood BMI Z-score. Multivariable regression modeling showed that OGTT values were associated with only sum of skinfolds and subscapular/triceps ratio and not with childhood BMI Z-score. Hispanic ethnicity and prepregnancy maternal BMI were most consistently related to childhood BMI Z-score and HOMA-IR, and Hispanic ethnicity with fasting glucose.Conclusions: Among women with untreated mild GDM and those without GDM, maternal glycemia is associated with childhood anthropometric measures of obesity but not childhood BMI, fasting glucose, or insulin resistance. Hispanic ethnicity, maternal BMI, and gestational weight gain were consistently related to childhood BMI.

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METHODS::Objective: Women with gestational diabetes (GDM) have a 7-12-fold increased risk for developing type 2 diabetes later in life. Postpartum weight retention is highly predictive for future obesity, and further increases risk for type 2 diabetes. We sought to identify predictors of losing at least 75% of gestational weight gain by very early postpartum in women with recent GDM.Methods: We recruited women with GDM during pregnancy or just after delivery. Prepregnancy weight was self-reported at recruitment; gestational weight gain, mode of delivery, and insulin use were extracted from medical records. At a mean of 7.2 (±2.1) weeks postpartum we measured weight and height and administered questionnaires, including demographics, breastfeeding, Edinburgh Postnatal Depression Scale, sleep, Harvard Food Frequency, and the International Physical Activity Questionnaire. We modeled the odds of 75% loss of gestational weight gain at the study visit using multivariable logistic regression models and selected the model with the lowest Akaike information criterion (AIC) as our final model. Analyses were conducted using JMP 10-13 Pro (SAS Institute Inc.)Results: Seventy-five women with recent GDM were included in the study. The mean age of study participants was 33 (SD ±5) years old, of whom 57% were white, 30% were African American, and 20% of the women identified as Hispanic. The mean prepregnancy BMI was 31.4 kg/m2 (SD ±5.6) and the mean pregnancy weight gain was 12.5 kg (SD ±7.8). Fifty-two percent of participants lost at least 75% of their pregnancy weight gain by the early postpartum study visit. Thirty-seven women (49%) exceeded Institute of Medicine (IOM) guidelines for gestational weight gain. In a multivariate model adjusting for weeks postpartum at the time of the study visit, less gestational weight gain (OR 0.56; 95% CI 0.39-0.73), increased age (OR 1.48; 95% CI 1.13-2.20), and lack of insulin use during pregnancy (OR 0.08 for use of insulin; 95% CI 0.00-0.73) were associated with at least 75% postpartum weight loss. Prepregnancy BMI and sleep were not retained in the model. Race/ethnicity, education, breastfeeding, nulliparity, cesarean section, depressive symptoms, dietary composition, glycemic index, and physical activity did not meet criteria for inclusion in the model.Conclusions: A substantial proportion of women with recent GDM lost at least 75% of their gestational weight gain by early postpartum. Older women, those who did not use insulin during pregnancy and those who gained less weight during pregnancy were significantly more likely to have lost 75% of gestational weight by very early postpartum.

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METHODS::Background: Low-glycemic index (GI) diet might be beneficial for gestational diabetes. However, the results remained controversial. We conducted a systematic review and meta-analysis to explore the influence of low-GI diet on gestational diabetes.Methods: PubMed, EMbase, Web of Science, EBSCO, and Cochrane library databases were systematically searched. Randomized controlled trials (RCTs) assessing the effect of low-GI diet on gestational diabetes were included. Two investigators independently searched articles, extracted data, and assessed the quality of included studies. This meta-analysis was performed using the random-effect model.Results: Six RCTs involving 532 patients were included in the meta-analysis. Overall, compared with a control intervention in gestational diabetes, low-GI diet was found to significantly reduce 2 h postprandial glucose (Std. MD = -0.46; 95% CI = -0.82 to -0.10; p = .01), but demonstrated no substantial influence on fasting plasma glucose (Std. MD = -0.24; 95% CI = -0.72 to 0.24; p = .33), HbA1c (Std. MD = 0.01; 95% CI = -0.29 to 0.31; p = .94), birth weight (Std. MD = -0.17; 95% CI = -0.41 to 0.06; p = .15), macrosomia (Std. MD = 0.45; 95% CI = 0.16 to 1.30; p = .14) and insulin requirement (Std. MD = 0.91; 95% CI = 0.68 to 1.22; p = .55).Conclusions: Compared with control intervention in gestational diabetes, low-GI diet was found to significantly decrease 2 h postprandial glucose, but showed no notable impact on fasting plasma glucose, HbA1c, birth weight, macrosomia, and insulin requirement.

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