BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China.
BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China; Hebei Technology Innovation Center of Human Settlement in Green Building, Shenzhen Institute of Building Research Co., Ltd., Xiongan, China.
Sci Total Environ. 2022 Jul 10;829:154657. doi: 10.1016/j.scitotenv.2022.154657. Epub 2022 Mar 18.
Ambient particulate matter (PM), especially its carbonaceous composition black carbon (BC) increases cardiometabolic risks, yet the underlying mechanisms are incompletely understood. Ceramides (Cer; a class of sphingolipids) are biological intermediates in glucose metabolism.
To explore whether Cer metabolism mediates impaired glucose homeostasis following short-term PM exposure.
In a panel study in Beijing, China, 112 participants were followed-up between 2016 and 2017. Targeted lipidomic analyses quantified 26 sphingolipids in 387 plasma samples. Ambient BC and PM with aerodynamic diameter ≤ 2.5 μm (PM) were continuously monitored in a station. We examined the associations of sphingolipid levels with average BC and PM concentrations 1-14 days before clinical visits using linear mixed-effects models, and explored the mediation effects of sphingolipids on PM-associated fasting blood glucose (FBG) difference using mediation analyses.
Increased levels of FBG and multiple sphingolipids in Cer metabolic pathways were associated with BC exposure in 1-14-day time window, but not with PM exposure. For each 10 μg/m increase in the average BC concentration 1-14 days before the clinical visits, species in the Cer C24:1 pathway (Cer, dihydroceramide, hexosylceramide, lactosylceramide, and sphingomyelin C24:1) increased in levels ranging from 11.8% (95% confidence interval [CI]: -6.2-33.2) to 48.7% (95% CI: 8.8-103.4), as did the Cer C16:0, C18:0, and C20:0 metabolic pathway species, ranging from 3.2% (95% CI: -5.6-12.9) to 32.4% (95% CI: 7.0-63.8), respectively. The Cer C24:1 metabolic pathway species mediated 6.5-25.5% of the FBG increase associated with BC exposure in 9-day time window. The Cer C16:0, C18:0, and C20:0 metabolic pathway species mediated 5.4-26.2% of the BC-associated FBG difference.
In conclusion, Cer metabolism may mediate impaired glucose homeostasis following short-term BC exposure. The current findings are preliminary, which need to be corroborated by further studies.
环境颗粒物（PM），尤其是其含碳成分黑碳（BC），会增加心血管代谢风险，但其中的机制尚不完全清楚。神经酰胺（Cer；一类神经鞘脂类）是葡萄糖代谢过程中的生物中间产物。
探索短期 PM 暴露后 Cer 代谢是否会导致葡萄糖稳态受损。
在中国北京的一项队列研究中，112 名参与者在 2016 年至 2017 年期间进行了随访。靶向脂质组学分析在 387 个血浆样本中定量了 26 种神经鞘脂。在一个站点连续监测环境 BC 和空气动力学直径≤2.5μm（PM）的 PM。我们使用线性混合效应模型，研究了在临床就诊前 1-14 天内，平均 BC 和 PM 浓度与 26 种神经鞘脂水平之间的关联，并通过中介分析探讨了神经鞘脂对 PM 相关空腹血糖（FBG）差异的中介作用。
在 1-14 天的时间窗内，与 BC 暴露相关的 FBG 升高和 Cer 代谢途径中的多种神经鞘脂水平升高，但与 PM 暴露无关。与临床就诊前 1-14 天内平均 BC 浓度每增加 10μg/m，Cer C24:1 途径中的物质（Cer、二氢神经酰胺、己糖神经酰胺、乳糖神经酰胺和神经鞘磷脂 C24:1）的水平分别增加 11.8%（95%置信区间 [CI]：-6.2-33.2）至 48.7%（95% CI：8.8-103.4），Cer C16:0、C18:0 和 C20:0 代谢途径的物质水平分别增加 3.2%（95% CI：-5.6-12.9）至 32.4%（95% CI：7.0-63.8）。Cer C24:1 代谢途径物质介导了 9 天时间窗内与 BC 暴露相关的 FBG 升高的 6.5%-25.5%。Cer C16:0、C18:0 和 C20:0 代谢途径物质介导了 BC 相关 FBG 差异的 5.4%-26.2%。
总之，Cer 代谢可能介导了短期 BC 暴露后葡萄糖稳态受损。目前的研究结果尚属初步，需要进一步研究证实。
