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胰岛细胞与胰岛素靶组织间的串扰通讯:冰山一角的隐藏面。

Crosstalk Communications Between Islets Cells and Insulin Target Tissue: The Hidden Face of Iceberg.

机构信息

Centre européen d'étude du Diabète, Unité Mixte de Recherche de l'Université de Strasbourg « Diabète et Thérapeutique », Strasbourg, France.

出版信息

Front Endocrinol (Lausanne). 2022 Feb 3;13:836344. doi: 10.3389/fendo.2022.836344. eCollection 2022.

DOI:10.3389/fendo.2022.836344
PMID:35185804
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8851682/
Abstract

The regulation of insulin secretion is under control of a complex inter-organ/cells crosstalk involving various metabolites and/or physical connections. In this review, we try to illustrate with current knowledge how β-cells communicate with other cell types and organs in physiological and pathological contexts. Moreover, this review will provide a better understanding of the microenvironment and of the context in which β-cells exist and how this can influence their survival and function. Recent studies showed that β-cell insulin secretion is regulated also by a direct and indirect inter-organ/inter-cellular communication involving various factors, illustrating the idea of "the hidden face of the iceberg". Moreover, any disruption on the physiological communication between β-cells and other cells or organs can participate on diabetes onset. Therefore, for new anti-diabetic treatments' development, it is necessary to consider the entire network of cells and organs involved in the regulation of β-cellular function and no longer just β-cell or pancreatic islet alone. In this context, we discuss here the intra-islet communication, the β-cell/skeletal muscle, β-cell/adipose tissue and β-cell/liver cross talk.

摘要

胰岛素分泌的调节受到涉及各种代谢物和/或物理连接的复杂器官/细胞间串扰的控制。在这篇综述中,我们试图用现有知识来说明β细胞在生理和病理情况下如何与其他细胞类型和器官进行通信。此外,这篇综述将提供对β细胞存在的微环境和背景的更好理解,以及这如何影响它们的存活和功能。最近的研究表明,β细胞胰岛素分泌也受到涉及各种因素的直接和间接器官/细胞间通讯的调节,说明了“冰山一角的隐藏面”的概念。此外,β细胞与其他细胞或器官之间的生理通讯的任何中断都可能参与糖尿病的发生。因此,为了开发新的抗糖尿病治疗方法,有必要考虑到参与调节β细胞功能的整个细胞和器官网络,而不仅仅是β细胞或胰岛本身。在这方面,我们在这里讨论了胰岛内的通讯、β细胞/骨骼肌、β细胞/脂肪组织和β细胞/肝脏的串扰。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e47/8851682/e2877b0e67d4/fendo-13-836344-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e47/8851682/e2877b0e67d4/fendo-13-836344-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e47/8851682/e2877b0e67d4/fendo-13-836344-g001.jpg

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Pro-inflammatory β cell small extracellular vesicles induce β cell failure through activation of the CXCL10/CXCR3 axis in diabetes.促炎的β 细胞小细胞外囊泡通过 CXCL10/CXCR3 轴激活诱导糖尿病中β 细胞衰竭。
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