Neuroendocrine hormone amylin in diabetes.

World J Diabetes

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.

Published: May 2016

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.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4856891PMC
http://dx.doi.org/10.4239/wjd.v7.i9.189DOI Listing

Publication Analysis

Top Keywords

human amylin
12
neuroendocrine hormone
8
hormone amylin
8
islet cells
8
fibrils amyloid
8
amyloid deposits
8
amylin
7
diabetes
4
amylin diabetes
4
diabetes neuroendocrine
4

Similar Publications

Background: High body mass index (BMI), which poorly represents specific fat depots, is linked to poorer cognition and higher dementia risk, with different associations between sexes. We examined associations of abdominal fat depots with cognition and brain volumes and whether sex modifies this association.

Method: 204 healthy middle-aged Alzheimer's-dementia (AD) offspring (mean age = 59.

View Article and Find Full Text PDF

Background: Varicella zoster virus (VZV) reactivation, manifesting as herpes zoster, increases dementia risk. Herein, we review the literature supporting the biological plausibility of VZV contributing to AD pathologies and examine the unique ability of VZV to induce amylin that has been found in blood vessels and parenchyma of AD patients.

Method: We conducted a literature review on VZV and dementia to elucidate a potential model for how VZV reactivation intersects with AD.

View Article and Find Full Text PDF

Public Health.

Alzheimers Dement

December 2024

Tulane National Primate Research Center, Tulane University, Coviington, LA, USA.

Background: Varicella zoster virus (VZV) is latent in ganglionic neurons in >90% of the world population and reactivates to produce herpes zoster in older adults. Zoster increases dementia risk, of which Alzheimer's disease (AD) is the most common. However, a critical barrier in studying the mechanisms by which VZV contributes to dementia is that VZV is an exclusively human virus.

View Article and Find Full Text PDF

Developing Topics.

Alzheimers Dement

December 2024

University of Kentucky, Lexington, KY, USA.

Background: Amylin is a systemic hormone that is co-secreted with insulin from pancreatic β-cells. Amylin co-aggregates with brain parenchymal and vascular β-amyloid in persons with Alzheimer's dementia. The present pilot study sought to assess the safety and side effects during and after the treatment period of passive amylin immunotherapy in the APP/PS1 mouse model of Alzheimer's disease.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!