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现在大家一起:胞吐作用或失败。

All together now: exocytose or fail.

机构信息

Institute of Physiology, Faculty of Medicine, University of Maribor, Slovenia.

出版信息

Islets. 2009 Jul-Aug;1(1):78-80. doi: 10.4161/isl.1.1.8757.

DOI:10.4161/isl.1.1.8757
PMID:21084853
Abstract

Compact and complex syncytium is a normal cellulo-social context for beta-cells within the healthy pancreatic islet. Optimal cell-to-cell electrical coupling through Connexin36 (Cx36) seems to ensure coordinated plasma membrane depolarization pattern and insulin exocytosis. Both phenomena can be further modulated by rich pancreas innervation. The complex structure and coordinated action develop after birth during fast hypertrophy and hyperplasia of the endocrine tissue and are maintained throughout adult life. The properties that emerge from the structure and coordination can disappear due to various reasons later in life and can lead to glucose intolerance and diabetes mellitus. In majority of cases the islet structure is lost after extensive beta-cell death in long-term hyperglycemia.

摘要

致密且复杂的合胞体是健康胰岛内β细胞的正常细胞间社会环境。通过连接蛋白 36(Cx36)实现的最佳细胞间电耦合似乎能确保协调的质膜去极化模式和胰岛素胞吐作用。这两种现象均可被丰富的胰腺神经支配进一步调节。这种复杂的结构和协调的作用在出生后内分泌组织的快速肥大和增生期间发展,并在整个成年期维持。从结构和协调中产生的特性可能由于各种原因在生命后期消失,并可能导致葡萄糖不耐受和糖尿病。在大多数情况下,在长期高血糖导致大量β细胞死亡后,胰岛结构丢失。

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All together now: exocytose or fail.现在大家一起:胞吐作用或失败。
Islets. 2009 Jul-Aug;1(1):78-80. doi: 10.4161/isl.1.1.8757.
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Loss of connexin36 channels alters beta-cell coupling, islet synchronization of glucose-induced Ca2+ and insulin oscillations, and basal insulin release.连接蛋白36通道的缺失会改变β细胞偶联、葡萄糖诱导的Ca2+和胰岛素振荡的胰岛同步性以及基础胰岛素释放。
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Functional connectivity in islets of Langerhans from mouse pancreas tissue slices.胰岛组织切片中胰岛的功能连接。
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