Review
Copyright ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Nov 6, 2022; 10(31): 11226-11239
Published online Nov 6, 2022. doi: 10.12998/wjcc.v10.i31.11226
Endocrine disruptor chemicals as obesogen and diabetogen: Clinical and mechanistic evidence
Niyazi Emre Kurşunoğlu, Banu Pinar Sarer Yurekli
Niyazi Emre Kurşunoğlu, School of Medicine, Ege University, İzmir 35100, Turkey
Banu Pinar Sarer Yurekli, Department of Endocrinology, Ege University School of Medicine, İzmir 35100, Turkey
Author contributions: Kurşunoğlu EN searched the literature, prepared the figures, wrote the manuscript, and edited the manuscript; Yürekli BS searched the literature, and edited the manuscript.
Conflict-of-interest statement: The authors have no conflict of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Banu Pinar Sarer Yurekli, MD, Associate Professor, Department of Endocrinology, Ege University School of Medicine, Ankara Street Bornova, İzmir 35100, Turkey. bsareryurekli@yahoo.com
Received: June 29, 2022
Peer-review started: June 29, 2022
First decision: August 1, 2022
Revised: August 19, 2022
Accepted: September 27, 2022
Article in press: September 27, 2022
Published online: November 6, 2022
Abstract

Obesity is becoming an inevitable pandemic all over the world. The World Obesity Federation predicts in the 2022 World Obesity Atlas that one billion people worldwide, including 1 in 5 women and 1 in 7 men, will be living with obesity by 2030. Moreover, the prevalence of diabetes is increasing worldwide, and diabetes is becoming more of a public health problem. Increased insulin resistance due to obesity and deficiency in insulin secretion are the two main causes of type 2 diabetes mellitus (T2DM). An exogenous chemical or mixture of chemicals that interferes with any aspect of hormone action was defined as endocrine-disrupting chemicals (EDCs). Bisphenol A (BPA), the first known EDC, was synthesized and was considered to be estrogenic. Global production of BPA has increased progressively from 5 to 8 million tons (MT) between 2010 and 2016. Furthermore, researchers estimated that the production should reach 10.2 MT by 2022. The human population is exposed to EDCs in daily life in such forms as pesticides/herbicides, industrial and household products, plastics, detergents, and personal care products. The term obesogen was used for chemicals that promote weight gain and obesity by increasing the number of adipocytes and fat storage in existing adipocytes, changing the energy balance, and finally regulating appetite and satiety. Besides the obesogenic effect, EDCs can cause T2DM through alteration in ß cell function and morphology and insulin resistance. In this review, we provide clinical and mechanistic evidence regarding EDCs as obesogen and diabetogen. However, those studies are not enough methodologically to indicate causality. In this respect, randomized clinical trials are needed to investigate the association between obesogen, diabetogen and the related metabolic clinical picture.

Keywords: Endocrine disruptors, Adipogenesis, Obesity, Diabetes mellitus

Core Tip: An exogenous chemical, or mixture of chemicals, that interferes with any aspect of hormone action was defined as Endocrine-Disrupting Chemicals (EDCs). Obesogens can promote obesity by increasing the number of adipocytes and fat storage in existing adipocytes, changing the calories burned at rest, changing the energy balance, and finally regulating satiety. Besides the obesogenic effect, EDCs can cause type 2 diabetes mellitus through alteration in ß cell function and morphology and insulin resistance. In this review, we provide clinical and mechanistic evidence regarding EDCs as obesogen and diabetogen.