Environmental endocrine disruptor-induced mitochondrial dysfunction: a potential mechanism underlying diabetes and its complications

Front Endocrinol (Lausanne). 2024 Aug 15:15:1422752. doi: 10.3389/fendo.2024.1422752. eCollection 2024.

Abstract

Diabetes and its complications significantly affect individuals' quality of life. The etiology of diabetes mellitus and its associated complications is complex and not yet fully understood. There is an increasing emphasis on investigating the effects of endocrine disruptors on diabetes, as these substances can impact cellular processes, energy production, and utilization, ultimately leading to disturbances in energy homeostasis. Mitochondria play a crucial role in cellular energy generation, and any impairment in these organelles can increase susceptibility to diabetes. This review examines the most recent epidemiological and pathogenic evidence concerning the link between endocrine disruptors and diabetes, including its complications. The analysis suggests that endocrine disruptor-induced mitochondrial dysfunction-characterized by disruptions in the mitochondrial electron transport chain, dysregulation of calcium ions (Ca2+), overproduction of reactive oxygen species (ROS), and initiation of signaling pathways related to mitochondrial apoptosis-may be key mechanisms connecting endocrine disruptors to the development of diabetes and its complications.

Keywords: diabetic complications; endocrine disruptor; mitochondrial dysfunction; reactive oxygen species; type 2 diabetes mellitus.

Publication types

  • Review

MeSH terms

  • Animals
  • Diabetes Complications / chemically induced
  • Diabetes Complications / metabolism
  • Diabetes Mellitus* / chemically induced
  • Diabetes Mellitus* / metabolism
  • Endocrine Disruptors* / adverse effects
  • Endocrine Disruptors* / toxicity
  • Environmental Exposure / adverse effects
  • Humans
  • Mitochondria* / drug effects
  • Mitochondria* / metabolism
  • Reactive Oxygen Species / metabolism

Substances

  • Endocrine Disruptors
  • Reactive Oxygen Species

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This study was funded by grant 82100040 from National Natural Science Foundation of China, grant 23A0662, 23B0872 from Scientific Research Foundation of Hunan Provincial Education Department, and grant 2022CYY012 from ESI Special Project of Changsha Medical University.