探索GIP对暴露于细胞因子的人类胰腺小岛和EndoC-βH5细胞的功能,保护和转录效应

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Updated: May 20, 2025

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

244

Kristine Henriksen1, Anne Jørgensen2, Simranjeet Kaur1

  • 1Translational Type 1 Diabetes Research, Department of Clinical and Translational Research, Steno Diabetes Center Copenhagen, Herlev, Denmark.

Molecular and cellular endocrinology
|March 23, 2025
PubMed
概括

葡萄糖依赖性胰岛素型多 (GIP) 以CaMK2依赖的方式增强胰岛素分泌,但不会保护人类β细胞免受细胞因子损伤. 在1型糖尿病模型中,GIP选择性调节炎症因子分泌.

关键词:
细胞灭亡 (apoptosis) 是一种死亡的过程.在EndoC-βH5中使用.在GIP的基础上,GIP是GIP.这是一种依赖葡萄糖的胰岛素型多.人类小岛屿的人类小岛屿在IFN-γ中使用IFN.一个IL-1ββ.有关炎症的细胞因子.第1类糖尿病患者.

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