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缺氧对GLP-1分泌的影响 - - 一项使用肠内分泌STC-1细胞作为模型的体外研究

Ravikant Sharma¹, Ghulam Shere Raza¹, Nalini Sodum¹

¹Research Unit of Biomedicine and Internal Medicine, Biocenter of Oulu, Medical Research Center, University of Oulu, Aapistie 5, 90220, Oulu, Finland.

Pflugers Archiv : European journal of physiology

|July 29, 2024

概括

缺氧通过降低GPR120和GPR40受体在肠内分泌细胞中的表达来降低营养刺激的葡萄糖样 (GLP) -1分泌. 基底GLP-1分泌仍不受低氧条件的影响.

科学领域:

内分泌学在内分泌学.
胃肠病学胃肠病学
细胞生物学细胞生物学

背景情况:

葡萄糖类 (GLP) -1 在摄入后由肠内分泌L细胞分泌.
L细胞通过G蛋白结合受体 (GPRs) 感知营养.
肠道L细胞经历过缺氧,原因是光线附近的氧气张力较低.

研究的目的:

为了研究缺氧对营养刺激GLP-1分泌的影响.
为了检查缺氧对STC-1细胞GPR表达的影响.
为了确定缺氧是否影响α-烯酸 (αLA) 诱导的GLP-1释放.

主要方法:

STC-1细胞被暴露在低氧 (1% O2) 中12小时.
细胞被用α-烯酸 (αLA) 处理以刺激GLP-1分泌.
测量了GLP-1分泌和GPR120/GPR40表达水平.

主要成果:

低氧并没有改变基底GLP-1分泌.
营养素 (αLA) 刺激的GLP-1分泌物在缺氧下显著减少 (45%的减少).
与normoxia相比,低氧降低了GPR120 (50%) 和GPR40 (60%) 的表达.

结论:

缺氧会影响营养刺激的GLP-1从肠内分泌细胞分泌.
缺氧下GLP-1分泌量的减少归因于GPR120和GPR40表达的减少.
肠道环境的变化和炎症可能会导致L细胞缺氧.

关键词:

肠内分泌细胞是内分泌细胞.脂肪酸是一种脂肪酸.这就是GLP-1.在 GPR40 和 GPR120 中,氧气过低是因为缺氧.

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