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Maternal metformin, obesity, and metabolic syndrome: The contribution of autonomic nervous system function

机译:孕妇二甲双胍,肥胖和代谢综合征:自主神经系统功能的贡献

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摘要

TO THE EDITORS: With great interest, we read the recent article by Desai et al regarding the effect of maternal met-formin treatment on fetal inflammation in a rat model of obesity and metabolic syndrome (MetS). The authors very clearly discussed the relation between metformin treatment and inflammation. They concluded that diet-induced obesity/ MetS during pregnancy significantly enhanced fetal and placental cytokine production. Maternal metformin reduced fetal cytokine levels, in addition; metformin treatment of a placental cell line suppressed tumor necrosis factor alpha-induced interleukin-6 levels by nuclear factor kappa B inhibitor. In addition to their fluent discussion, we aimed to emphasize the possible other effective mechanism of metformin treatment on MetS and obesity: the contribution of autonomic nervous system function.
机译:致编辑:我们非常感兴趣,我们阅读了Desai等人的最新文章,内容涉及母体二甲双胍治疗对肥胖症和代谢综合征(MetS)大鼠模型中胎儿炎症的影响。作者非常清楚地讨论了二甲双胍治疗与炎症之间的关系。他们得出结论,怀孕期间饮食引起的肥胖/ MetS显着增强了胎儿和胎盘细胞因子的产生。孕妇二甲双胍可降低胎儿细胞因子水平。二甲双胍对胎盘细胞系的治疗通过核因子κB抑制剂抑制了肿瘤坏死因子α诱导的白介素6水平。除了他们的流畅讨论之外,我们旨在强调二甲双胍治疗MetS和肥胖症的其他可能有效机制:自主神经系统功能的贡献。

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