肥胖及其相关脂肪酸对胎盘炎症的影响。
The Influence of Obesity and Associated Fatty Acids on Placental Inflammation.
机构信息
Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Department of Chemistry, Vanderbilt University, Nashville, TN, USA.
出版信息
Clin Ther. 2021 Feb;43(2):265-278. doi: 10.1016/j.clinthera.2020.12.018. Epub 2021 Jan 21.
PURPOSE
Maternal obesity, affecting nearly 1 in 4 pregnancies, is associated with increased circulating saturated fatty acids, such as palmitate. These fatty acids are implicated in placental inflammation, which may in turn exacerbate both maternal-fetal tolerance and responses to pathogens, such as group B Streptococcus. In this review, we address the question, "How do obesity and associated fatty acids influence placental inflammation?"
METHODS
In this narrative review, we searched PubMed and Google Scholar using combinations of the key words placental inflammation or pregnancy and lipids, fatty acids, obesity, palmitate, or other closely related search terms. We also used references found within these articles that may have been absent from our original search queries. We analyzed methods and key results of these articles to compare and contrast their findings, which were occasionally at odds with each other.
FINDINGS
Although obesity can be studied as a whole, complex phenomena with in vivo mouse models and human samples from patients with obesity, in vitro modeling often relies on the treatment of cells or tissues with ≥1 fatty acids and occasionally other compounds (eg, glucose and insulin). We found that palmitate, most commonly used in vitro to recreate hallmarks of obesity, induces apoptosis, oxidative stress, mitochondrial dysfunction, autophagy defects, and inflammasome activation in many placental cell types. We compare this to in vivo models of obesity wherever possible. We found that obesity as a whole may have more complex regulation of these phenomena (apoptosis, oxidative stress, mitochondrial dysfunction, autophagy defects, and inflammasome activation) compared with in vitro models of fatty acid treatment (primarily palmitate) because of the presence of unsaturated fatty acids (ie, oleate), which may have anti-inflammatory effects.
IMPLICATIONS
The interaction of unsaturated fatty acids with saturated fatty acids may ameliorate many inflammatory effects of saturated fatty acids alone, which complicates interpretation of in vitro studies that focus on a particular fatty acid in isolation. This complication may explain why certain studies of obesity in vivo have differing outcomes from studies of specific fatty acids in vitro.
目的
肥胖症影响了近四分之一的妊娠，与循环中饱和脂肪酸（如棕榈酸）的增加有关。这些脂肪酸与胎盘炎症有关，而胎盘炎症反过来又可能加剧母体-胎儿耐受和对病原体（如 B 族链球菌）的反应。在这篇综述中，我们提出了一个问题：“肥胖症和相关脂肪酸如何影响胎盘炎症？”
方法
在这篇叙述性综述中，我们使用了“胎盘炎症或妊娠”和“脂质、脂肪酸、肥胖症、棕榈酸或其他密切相关的搜索词”的组合，在 PubMed 和 Google Scholar 上进行了搜索。我们还使用了这些文章中可能没有包含在我们原始搜索查询中的参考文献。我们分析了这些文章的方法和关键结果，以比较和对比它们的发现，这些发现有时相互矛盾。
发现
尽管肥胖症可以作为一个整体进行研究，但在体内小鼠模型和肥胖症患者的人体样本中，复杂的现象需要使用细胞或组织与≥1 种脂肪酸和偶尔的其他化合物（如葡萄糖和胰岛素）进行处理。我们发现，棕榈酸，最常用于体外重现肥胖症的特征，可诱导许多胎盘细胞类型的细胞凋亡、氧化应激、线粒体功能障碍、自噬缺陷和炎症小体激活。我们尽可能地将其与肥胖症的体内模型进行比较。我们发现，与体外模型的脂肪酸处理（主要是棕榈酸）相比，肥胖症作为一个整体可能对这些现象（细胞凋亡、氧化应激、线粒体功能障碍、自噬缺陷和炎症小体激活）有更复杂的调控，因为存在不饱和脂肪酸（即油酸），可能具有抗炎作用。
影响
不饱和脂肪酸与饱和脂肪酸的相互作用可能会减轻饱和脂肪酸单独引起的许多炎症作用，这使得单独研究特定脂肪酸的体外研究的解释变得复杂。这种复杂性可能解释了为什么某些肥胖症的体内研究与特定脂肪酸的体外研究结果不同。
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