关键词: Ca2+ signaling dedifferentiation gene expression metabolic stress pancreatic β-cells type 2 diabetes

Mesh : Insulin-Secreting Cells / metabolism pathology Humans Calcium Signaling / physiology Animals Stress, Physiological / physiology Diabetes Mellitus, Type 2 / metabolism Calcium / metabolism Insulin Resistance / physiology

来  源:   DOI:10.3389/fendo.2024.1412411   PDF(Pubmed)

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 Ca2+ concentration ([Ca2+]i), 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 [Ca2+]i impairs β-cell function.
摘要:
早期的2型糖尿病(T2D)的发展,胰岛素抵抗和营养超负荷引起的代谢应激引起β细胞过度刺激。在这里,我们总结了最近的研究,探索了细胞内Ca2+浓度增加的前提([Ca2+]i),由β细胞持续的代谢刺激引起,通过对β细胞功能产生不利影响而导致β细胞功能障碍和衰竭,结构,和身份。这篇小型评论建立在最近的几篇评论的基础上,这些评论还描述了过量的[Ca2]i如何损害β细胞功能。
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