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Targeted lipidomics and transcriptomics data of white adipose tissue under ER stress

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doi.org2025-03-23 收录
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http://doi.org/10.17632/sy8gyx2bmx.1
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Endoplasmic reticulum (ER) stress is known to impair the function of visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT), disrupting lipid metabolism. Despite the crucial role lipid plays in regulating adipose tissue function, the specific lipidomic alterations in VAT and SAT under ER stress remain unclear. In this study, ER stress was induced in VAT and SAT, and targeted lipidomic and transcriptomic approaches were applied to assess the profiles of lipid metabolism and gene expression under ER stress condition. . The results revealed that VAT displayed a more pronounced ER stress response, including a marked increase in binding immunoglobulin protein (BiP) expression, and significant lipidomic disruptions, particularly in glycerides and sterols. These disruptions involved a reduction in protective polyunsaturated fatty acyl species and the accumulation of lipotoxic molecules. While SAT exhibited less severe disruptions in lipid metabolism. Transcriptomic analysis further revealed tissue-specific gene expression patterns, with VAT being more susceptible to immune activation, inflammation and metabolic dysfunction, while SAT exhibited alterations predominantly in protein folding processes. These findings provide critical insights into tissue-specific mechanisms of ER stress adaptation in adipose tissues, positioning VAT as a potential therapeutic target for addressing metabolic dysfunction in obesity-related disorders.

内质网(ER)应激已被证实会损害内脏脂肪组织(VAT)和皮下脂肪组织(SAT)的功能,进而扰乱脂质代谢。尽管脂质在调节脂肪组织功能中扮演着至关重要的角色,但在内质网应激条件下,VAT和SAT中特定的脂质组学改变仍不明确。在本研究中,通过在VAT和SAT中诱导内质网应激,并采用针对性的脂质组学和转录组学方法,对脂质代谢和基因表达在内质网应激条件下的特征进行了评估。研究结果揭示,VAT表现出更为明显的内质网应激反应,包括结合免疫球蛋白蛋白(BiP)表达的显著增加,以及显著的脂质组学紊乱,尤其是在甘油三酯和甾醇方面。这些紊乱包括保护性多不饱和脂肪酸酰基种类的减少和脂毒性分子的积累。而SAT在脂质代谢方面的紊乱则相对较轻。转录组学分析进一步揭示了组织特异性的基因表达模式,其中VAT对免疫激活、炎症和代谢功能障碍更为敏感,而SAT则主要表现出蛋白质折叠过程的改变。这些发现为脂肪组织中内质网应激适应的组织特异性机制提供了关键的见解,并将VAT定位为针对肥胖相关疾病中代谢功能障碍的潜在治疗靶点。
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