Zhang XX, Pan YH, Huang YM, Zhao HL. Neuroendocrine hormone amylin in diabetes. World J Diabetes 2016; 7(9): 189-197 [PMID: 27162583 DOI: 10.4239/wjd.v7.i9.189]
Corresponding Author of This Article
Hai-Lu Zhao, MD, PhD, Professor, Director, Centre of Diabetic Systems Medicine, Guangxi Key Laboratory of Excellence, Guilin Medical University, Huan Cheng North 2nd Road 109, Guilin 541004, Guangxi Zhuang Autonomous Region, China. zhaohailu9@126.com
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Xiao-Xi Zhang, Yan-Hong Pan, Yan-Mei Huang, Hai-Lu Zhao, Centre of Diabetic Systems Medicine, Guangxi Key Laboratory of Excellence, Guilin Medical University, Guilin 541004, Guangxi Zhuang Autonomous Region, China
Xiao-Xi Zhang, Hai-Lu Zhao, Institute of Basic Medical Science, College of Basic Medical Science, Guilin Medical University, Guilin 541004, Guangxi Zhuang Autonomous Region, China
Author contributions: Zhang XX performed the majority of the writing, prepared the figures and tables; Pan YH performed data accusation and writing; Huang YM provided the information of tables of the paper; Zhao HL designed the outline and coordinated the writing of the paper.
Conflict-of-interest statement: There is no conflict of interest associated with any of the senior author or other coauthors contributed their efforts in this manuscript.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Hai-Lu Zhao, MD, PhD, Professor, Director, Centre of Diabetic Systems Medicine, Guangxi Key Laboratory of Excellence, Guilin Medical University, Huan Cheng North 2nd Road 109, Guilin 541004, Guangxi Zhuang Autonomous Region, China. zhaohailu9@126.com
Telephone: +86-773-5805803 Fax: +86-773-5895805
Received: January 6, 2016 Peer-review started: January 9, 2016 First decision: March 1, 2016 Revised: March 16, 2016 Accepted: April 5, 2016 Article in press: April 6, 2016 Published online: May 10, 2016
Abstract
The neuroendocrine hormone amylin, also known as islet amyloid polypeptide, is co-localized, co-packaged and co-secreted with insulin from adult pancreatic islet β cells to maintain glucose homeostasis. Specifically, amylin reduces secretion of nutrient-stimulated glucagon, regulates blood pressure with an effect on renin-angiotensin system, and delays gastric emptying. The physiological actions of human amylin attribute to the conformational α-helix monomers whereas the misfolding instable oligomers may be detrimental to the islet β cells and further transform to β-sheet fibrils as amyloid deposits. No direct evidence proves that the amylin fibrils in amyloid deposits cause diabetes. Here we also have performed a systematic review of human amylin gene changes and reported the S20G mutation is minor in the development of diabetes. In addition to the metabolic effects, human amylin may modulate autoimmunity and innate inflammation through regulatory T cells to impact on both human type 1 and type 2 diabetes.
Core tip: This is a systematic review to describe amylin as a neuroendocrine hormone. Besides the glucose homeostasis and cytotoxicity of amylin, we tried to perform that the S20G mutation of human amylin is also minor in the pathogenesis of diabetes. In addition to the metabolic effects, human amylin may have impact on autoimmunity, implicating a potential as the immunosuppressor to improve autoimmunity conditions in the future therapy of diabetes, allergic diseases and immune rejection.
