Intensive lactation among women with recent gestational diabetes significantly alters the early postpartum circulating lipid profile: the SWIFT study.
Intensive lactation among women with recent gestational diabetes significantly alters the early postpartum circulating lipid profile: the SWIFT study.
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DOI：
10.1186/s12916-021-02095-1
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发表时间：
2021-10-08
期刊：
影响因子：
9.3
通讯作者：
Gunderson EP
中科院分区：
文献类型：
--
作者：
Zhang Z;Lai M;Piro AL;Alexeeff SE;Allalou A;Röst HL;Dai FF;Wheeler MB;Gunderson EP
有妊娠糖尿病（GDM）病史的女性患2型糖尿病（T2 D）的风险高7倍。据估计，20-50%有GDM病史的女性将在分娩后10年内进展为T2 D。密集的哺乳可能与这种风险呈负相关，但保护作用背后的机制仍然未知。在这项研究中，我们使用了一个前瞻性GDM队列，其中包括1010名产后6-9周（研究基线）未患T2 D的女性，并对基线后8年内的T2 D发作进行了检测（n=980）。对350名女性（216名强化母乳喂养，IBF vs. 134名强化配方奶粉喂养或混合喂养，IFF/Mixed）在研究检查期间在基线和随访（基线后1-2年）时采集的空腹血浆样本进行靶向代谢分析。评价了基线和随访时泌乳强度与循环代谢物之间的关系，以发现泌乳的潜在代谢反应，并探索这些代谢物与T2 D风险之间的联系。我们观察到泌乳强度与基线时的甘油脂（TAG/DAG）降低和磷脂/鞘脂增加密切相关。这种脂质特征表明，从甘油脂质代谢途径向磷脂/鞘脂代谢途径转变导致脂肪生成减少，这是哺乳获益机制的一个组成部分。纵向分析表明，这种有利的脂质分布是短暂的，并在产后1-2年减少，与哺乳期停止一致。重要的是，当在随访期间按未来T2 D状态对这350名女性进行分层时（171名未来T2 D vs. 179名无T2 D），我们发现哺乳仅在未发生T2 D事件的女性中引起强烈的脂质变化。随后，我们鉴定了与未来T2 D风险强烈相关的代谢物簇，从中我们开发了具有0.78的区分能力（AUC）的预测代谢特征，其上级于常见的临床变量（即，空腹血糖，AUC 0.56或2小时血糖，AUC 0.62）。在这项研究中，我们表明，密集的哺乳期显着改变了循环脂质在产后早期，谁不对哺乳代谢的妇女更有可能发展为T2 D。我们还发现了一个10种分析物的代谢特征，能够预测未来发生的T2 D的IBF妇女。我们的研究结果为哺乳如何影响母体代谢及其与未来糖尿病发病的联系提供了新的见解。ClinicalTrials.gov NCT01967030。在线版本包含补充材料，可通过10.1186/s12916-021-02095-1获得。
Women with a history of gestational diabetes mellitus (GDM) have a 7-fold higher risk of developing type 2 diabetes (T2D). It is estimated that 20-50% of women with GDM history will progress to T2D within 10 years after delivery. Intensive lactation could be negatively associated with this risk, but the mechanisms behind a protective effect remain unknown. In this study, we utilized a prospective GDM cohort of 1010 women without T2D at 6-9 weeks postpartum (study baseline) and tested for T2D onset up to 8 years post-baseline (n=980). Targeted metabolic profiling was performed on fasting plasma samples collected at both baseline and follow-up (1-2 years post-baseline) during research exams in a subset of 350 women (216 intensive breastfeeding, IBF vs. 134 intensive formula feeding or mixed feeding, IFF/Mixed). The relationship between lactation intensity and circulating metabolites at both baseline and follow-up were evaluated to discover underlying metabolic responses of lactation and to explore the link between these metabolites and T2D risk. We observed that lactation intensity was strongly associated with decreased glycerolipids (TAGs/DAGs) and increased phospholipids/sphingolipids at baseline. This lipid profile suggested decreased lipogenesis caused by a shift away from the glycerolipid metabolism pathway towards the phospholipid/sphingolipid metabolism pathway as a component of the mechanism underlying the benefits of lactation. Longitudinal analysis demonstrated that this favorable lipid profile was transient and diminished at 1-2 years postpartum, coinciding with the cessation of lactation. Importantly, when stratifying these 350 women by future T2D status during the follow-up (171 future T2D vs. 179 no T2D), we discovered that lactation induced robust lipid changes only in women who did not develop incident T2D. Subsequently, we identified a cluster of metabolites that strongly associated with future T2D risk from which we developed a predictive metabolic signature with a discriminating power (AUC) of 0.78, superior to common clinical variables (i.e., fasting glucose, AUC 0.56 or 2-h glucose, AUC 0.62). In this study, we show that intensive lactation significantly alters the circulating lipid profile at early postpartum and that women who do not respond metabolically to lactation are more likely to develop T2D. We also discovered a 10-analyte metabolic signature capable of predicting future onset of T2D in IBF women. Our findings provide novel insight into how lactation affects maternal metabolism and its link to future diabetes onset. ClinicalTrials.gov NCT01967030. The online version contains supplementary material available at 10.1186/s12916-021-02095-1.
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影响因子：
7.7
作者：
Gunderson EP;Jacobs DR Jr;Chiang V;Lewis CE;Feng J;Quesenberry CP Jr;Sidney S
通讯作者：
Sidney S
影响因子：
7.7
作者：
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影响因子：
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