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腺苷、肾上腺素能和阿片途径在胰岛素分泌、β 细胞增殖和再生的调节中的作用。

The adenosine, adrenergic and opioid pathways in the regulation of insulin secretion, beta cell proliferation and regeneration.

机构信息

Deakin University, School of Medicine, Faculty of Health, 75 Pigdons Rd, Waurn Ponds, Geelong, VIC, 3216, Australia.

Deakin University, School of Medicine, Faculty of Health, 75 Pigdons Rd, Waurn Ponds, Geelong, VIC, 3216, Australia.

出版信息

Pancreatology. 2018 Sep;18(6):615-623. doi: 10.1016/j.pan.2018.06.006. Epub 2018 Jun 20.

DOI:10.1016/j.pan.2018.06.006
PMID:29937364
Abstract

Insulin, a key hormone produced by pancreatic beta cells precisely regulates glucose metabolism in vertebrates. In type 1 diabetes, the beta cell mass is destroyed, a process triggered by a combination of environmental and genetic factors. This ultimately results in absolute insulin deficiency and dysregulated glucose metabolism resulting in a number of detrimental pathophysiological effects. The traditional focus of treating type 1 diabetes has been to control blood sugar levels through the administration of exogenous insulin. Newer approaches aim to replace the beta cell mass through pancreatic or islet transplantation. Type 2 diabetes results from a relative insulin deficiency for the prevailing insulin resistance. Treatments are generally aimed at reducing insulin resistance and/or augmenting insulin secretion and the use of insulin itself is often required. It is increasingly being recognized that the beta cell mass is dynamic and increases insulin secretion in response to beta cell mitogens and stress signals to maintain glycemia within a very narrow physiological range. This review critically discusses the role of adrenergic, adenosine and opioid pathways and their interrelationship in insulin secretion, beta cell proliferation and regeneration.

摘要

胰岛素是由胰腺β细胞产生的关键激素,它在脊椎动物中精确调节葡萄糖代谢。在 1 型糖尿病中,β细胞数量减少,这一过程是由环境和遗传因素共同引发的。这最终导致绝对胰岛素缺乏和葡萄糖代谢失调,导致许多不利的病理生理效应。治疗 1 型糖尿病的传统重点一直是通过外源性胰岛素来控制血糖水平。较新的方法旨在通过胰腺或胰岛移植来替代β细胞数量。2 型糖尿病是由于胰岛素抵抗导致相对胰岛素缺乏引起的。治疗方法通常旨在降低胰岛素抵抗和/或增强胰岛素分泌,并且经常需要使用胰岛素本身。人们越来越认识到,β细胞数量是动态的,它会响应β细胞有丝分裂原和应激信号增加胰岛素分泌,以将血糖维持在非常狭窄的生理范围内。这篇综述批判性地讨论了肾上腺素能、腺苷和阿片途径及其在胰岛素分泌、β细胞增殖和再生中的相互关系。

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