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睑板腺脂质组学分析在 1 型糖尿病小鼠模型中的研究及潜在机制的初步研究。

Lipidomic analysis of meibomian glands from type-1 diabetes mouse model and preliminary studies of potential mechanism.

机构信息

Department of Medicine, Qingdao University, Qingdao, China; State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong First Medical University & Shandong Academy of Medical Sciences, Qingdao, China.

Qingdao Eye Hospital of Shandong First Medical University, Qingdao, China; State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong First Medical University & Shandong Academy of Medical Sciences, Qingdao, China.

出版信息

Exp Eye Res. 2021 Sep;210:108710. doi: 10.1016/j.exer.2021.108710. Epub 2021 Jul 30.

DOI:10.1016/j.exer.2021.108710
PMID:34339682
Abstract

Diabetes is a significant risk factor for meibomian gland dysfunction (MGD), but its mechanism is poorly understood. The main function of the meibomian glands (MGs) is to synthesize, store, and secrete lipids. In this study, we found that the amount of lipids in the meibomian acini in STZ-induced type 1 diabetic mice decreased, and the lipid droplets became larger and irregular. In all, 31 lipid subclasses were identified in the mouse MGs, which contained 1378 lipid species in total through lipidomics analysis based on LC-MS/MS. Diabetes caused a significant increase in the content of ceramides (Cer) in the MGs but a significant decrease in the ration of sphingomyelin to ceramides (SM/Cer). The quantity of meibocytes in diabetic mice was dramatically decreased, and the proliferation activity was alleviated, which may be associated with cell cycle arrest caused by diabetes-induced abnormal Cer metabolism in MGs. We found an increase in macrophage and neutrophils infiltration in the diabetic MGs, which may be related to the significant reduction of AcCa in diabetic MGs. Taken together, the results of the present study demonstrated that diabetes induced disruption of lipid homeostasis in MGs, which may mediate the decreased cell proliferation and increased inflammation caused by diabetes in MGs.

摘要

糖尿病是睑板腺功能障碍(MGD)的一个重要危险因素,但它的发病机制尚不清楚。睑板腺(MGs)的主要功能是合成、储存和分泌脂质。在这项研究中,我们发现 STZ 诱导的 1 型糖尿病小鼠的睑板腺中脂质的含量减少,并且脂质滴变得更大和不规则。通过基于 LC-MS/MS 的脂质组学分析,总共在小鼠 MGs 中鉴定出 31 种脂质亚类,总共包含 1378 种脂质。糖尿病导致 MGs 中的神经酰胺(Cer)含量显著增加,但鞘磷脂与神经酰胺的比例(SM/Cer)显著降低。糖尿病小鼠的睑板腺细胞数量明显减少,增殖活性减轻,这可能与糖尿病引起的 MGs 中异常 Cer 代谢引起的细胞周期停滞有关。我们发现糖尿病 MGs 中巨噬细胞和中性粒细胞浸润增加,这可能与糖尿病 MGs 中 AcCa 的显著减少有关。综上所述,本研究结果表明,糖尿病诱导 MGs 中的脂质稳态紊乱,可能介导糖尿病引起的 MGs 中细胞增殖减少和炎症增加。

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