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钙信号传导与代谢应激诱导的胰腺β细胞功能衰竭。

Ca signaling and metabolic stress-induced pancreatic β-cell failure.

作者信息

Magnuson Mark A, Osipovich Anna B

机构信息

Department of Molecular Physiology and Biophysics and Center for Stem Cell Biology, Vanderbilt University, Nashville, TN, United States.

出版信息

Front Endocrinol (Lausanne). 2024 Jul 2;15:1412411. doi: 10.3389/fendo.2024.1412411. eCollection 2024.

Abstract

Early in the development of Type 2 diabetes (T2D), metabolic stress brought on by insulin resistance and nutrient overload causes β-cell hyperstimulation. Herein we summarize recent studies that have explored the premise that an increase in the intracellular Ca concentration ([Ca]), brought on by persistent metabolic stimulation of β-cells, causes β-cell dysfunction and failure by adversely affecting β-cell function, structure, and identity. This mini-review builds on several recent reviews that also describe how excess [Ca] impairs β-cell function.

摘要

在2型糖尿病(T2D)发展早期,胰岛素抵抗和营养过剩所引发的代谢应激会导致β细胞过度刺激。在此,我们总结了近期的研究,这些研究探讨了这样一个前提:β细胞持续受到代谢刺激导致细胞内钙离子浓度([Ca])升高,通过对β细胞功能、结构和特性产生不利影响,进而导致β细胞功能障碍和衰竭。这篇小型综述建立在近期其他几篇综述的基础之上,那些综述也描述了过量的[Ca]如何损害β细胞功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1943/11250477/121989511e7d/fendo-15-1412411-g001.jpg

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