Maternal overweight is not an independent risk factor for increased birth weight, leptin and insulin in newborns of gestational diabetic women: observations from the prospective 'EaCH' cohort study.
Maternal overweight is not an independent risk factor for increased birth weight, leptin and insulin in newborns of gestational diabetic women: observations from the prospective 'EaCH' cohort study.
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DOI：
10.1186/s12884-018-1889-8
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发表时间：
2018-06-20
影响因子：
3.1
通讯作者：
Plagemann A
中科院分区：
文献类型：
--
作者：
Ott R;Stupin JH;Loui A;Eilers E;Melchior K;Rancourt RC;Schellong K;Ziska T;Dudenhausen JW;Henrich W;Plagemann A
妊娠期糖尿病（GDM）和孕期超重/肥胖都是有害的人体测量和激素新生儿结局的危险因素，后来被确定为“计划”不良健康倾向。虽然超重/肥胖是GDM的主要决定因素，但对关键出生结局的独立影响尚不清楚。因此，本研究的目的是评估在患有GDM的女性中，超重/肥胖与改变的糖代谢对新生儿参数的相对/独立影响。前瞻性观察性“早期CHARITÉ （EaCH）”队列研究主要关注通过产前和/或产后早期暴露于“致糖尿病/致脂肪”环境而导致的不良健康结果的早期发育起源。该研究包括2007年至2010年间招募的205对母子，他们都是在德国柏林慈善医院（charity - Universitätsmedizin）产科诊所接受GDM治疗并分娩的妇女。招募、治疗、代谢物/激素分析和数据评估均按照标准化指南和方案进行。本报告特别旨在确定产妇的人体测量和代谢决定因素的人体测量和关键激素分娩结果在“每”。组间比较、Spearman相关和未调整线性回归分析初步证实，孕妇孕前身体质量指数（BMI）升高是新生儿体重、脐带血胰岛素和瘦素升高的重要因素（均P < 0.05）。然而，在妊娠后期对母体葡萄糖的考虑和调整表明，母体的人体测量参数（体重、BMI、妊娠期体重增加）均无显著变化（所有n.s）。相比之下，即使在调整了母体人体测量值后，妊娠晚期的血糖值（妊娠第32周和第36周的空腹和餐后血糖，妊娠晚期和分娩时的糖化血红蛋白）与关键分娩结局明显呈正相关（均P < 0.05）。超重/肥胖和妊娠期体重增加似乎都不是出生体重、胰岛素和瘦素增加的独立决定因素。相反，妊娠晚期血糖似乎对各自的新生儿结局至关重要。因此，妊娠期护理和未来的研究应充分考虑伴有或不伴有GDM的超重/肥胖妇女妊娠后期的血糖，以评估后代“围产期糖尿病”的关键原因和干预策略。
Both gestational diabetes mellitus (GDM) as well as overweight/obesity during pregnancy are risk factors for detrimental anthropometric and hormonal neonatal outcomes, identified to ‘program’ adverse health predispositions later on. While overweight/obesity are major determinants of GDM, independent effects on critical birth outcomes remain unclear. Thus, the aim of the present study was to evaluate, in women with GDM, the relative/independent impact of overweight/obesity vs. altered glucose metabolism on newborn parameters. The prospective observational ‘Early CHARITÉ (EaCH)’ cohort study primarily focuses on early developmental origins of unfavorable health outcomes through pre- and/or early postnatal exposure to a ‘diabetogenic/adipogenic’ environment. It includes 205 mother-child dyads, recruited between 2007 and 2010, from women with treated GDM and delivery at the Clinic of Obstetrics, Charité – Universitätsmedizin Berlin, Germany. Recruitment, therapy, metabolite/hormone analyses, and data evaluation were performed according to standardized guidelines and protocols. This report specifically aimed to identify maternal anthropometric and metabolic determinants of anthropometric and critical hormonal birth outcomes in ‘EaCH’. Group comparisons, Spearman’s correlations and unadjusted linear regression analyses initially confirmed that increased maternal prepregnancy body-mass-index (BMI) is a significant factor for elevated birth weight, cord-blood insulin and leptin (all P < 0.05). However, consideration of and adjustment for maternal glucose during late pregnancy showed that no maternal anthropometric parameter (weight, BMI, gestational weight gain) remained significant (all n.s.). In contrast, even after adjustment for maternal anthropometrics, third trimester glucose values (fasting and postprandial glucose at 32nd and 36th weeks’ gestation, HbA1c in 3rd trimester and at delivery), were clearly positively associated with critical birth outcomes (all P < 0.05). Neither overweight/obesity nor gestational weight gain appear to be independent determinants of increased birth weight, insulin and leptin. Rather, 3rd trimester glycemia seems to be crucial for respective neonatal outcomes. Thus, gestational care and future research studies should greatly consider late pregnancy glucose in overweight/obese women with or without GDM, for evaluation of critical causes and interventional strategies against ‘perinatal programming of diabesity’ in the offspring.
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影响因子：
120.7
作者：
Flegal, Katherine M.;Carroll, Margaret D.;Curtin, Lester R.
通讯作者：
Curtin, Lester R.
在具有良好的1型糖尿病和良好血糖控制的女性中，大糖症的风险仍然依赖于葡萄糖。
影响因子：
3.7
作者：
Cyganek K;Skupien J;Katra B;Hebda-Szydlo A;Janas I;Trznadel-Morawska I;Witek P;Kozek E;Malecki MT
通讯作者：
Malecki MT
影响因子：
16.2
作者：
Black MH;Sacks DA;Xiang AH;Lawrence JM
通讯作者：
Lawrence JM
影响因子：
8
作者：
Boney, CM;Verma, A;Vohr, BR
通讯作者：
Vohr, BR
影响因子：
9.3
作者：
Ensenauer, Regina;Brandlhuber, Lena;von Kries, Ruediger
通讯作者：
von Kries, Ruediger