Abstract
Endocrine disrupting chemicals (EDCs) can mimic natural hormone to interact with receptors in the endocrine system and thus disrupt the functions of the endocrine system, raising concerns on the public health. In addition to disruption of the endocrine system, some EDCs have been found associated with many diseases such as breast cancer, prostate cancer, infertility, asthma, stroke, Alzheimer’s disease, obesity, and diabetes mellitus. EDCs that binding androgen receptor have been reported associated with diabetes mellitus in in vitro, animal, and clinical studies. In this review, we summarize the structural basis and interactions between androgen receptor and EDCs as well as the associations of various types of diabetes mellitus with the EDCs mediated through androgen receptor binding. We also discuss the perspective research for further understanding the impact and mechanisms of EDCs on the risk of diabetes mellitus.
Highlights
Endocrine disrupting chemicals (EDCs) can mimic natural hormone to interact with receptors in the endocrine system and disrupt the functions of the endocrine system, raising concerns on the public health
There are more than 340 million people worldwide affected by diabetes mellitus and this number is projected to be double by the year 2025 [3]
Exposure to Bisphenol A (BPA) leads to insulin resistance which results in Type 2 diabetes mellitus (T2DM) through the highly expressed pancreatic β cells [100]
Summary
Diabetes mellitus are described as a complex and serious condition of metabolic disease associated with abnormally high levels of blood sugar (glucose) resulting from deficiency of insulin secretion and/or action. Type 1 diabetes mellitus (T1DM) is an autoimmune condition in which the immune system is activated to destroy the cells in the pancreas which produce insulin. Type 2 diabetes mellitus (T2DM) is a progressive condition in which the body becomes resistant to the normal effects of insulin and/or gradually loses the capacity to produce enough insulin in the pancreas [1]. Receptor in β cells, which increases cellular cyclic adenosine monophosphate (cAMP) levels and amplifies the incretin effect of GLP-1 [14]
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