Inappropriately sweet: Environmental endocrine-disrupting chemicals and the diabetes pandemic

Abstract

Afflicting hundreds of millions of individuals globally, diabetes mellitus is a chronic disorder of energy metabolism characterized by hyperglycemia and other metabolic derangements that result in significant individual morbidity and mortality as well as substantial healthcare costs. Importantly, the impact of diabetes in the United States is not uniform across the population; rather, communities of color and those with low income are disproportionately affected. While excessive caloric intake, physical inactivity, and genetic susceptibility are undoubted contributors to diabetes risk, these factors alone fail to fully explain the rapid global rise in diabetes rates. Recently, environmental contaminants acting as endocrine-disrupting chemicals (EDCs) have been implicated in the pathogenesis of diabetes. Indeed, burgeoning data from cell-based, animal, population, and even clinical studies now indicate that a variety of structurally distinct EDCs of both natural and synthetic origin have the capacity to alter insulin secretion and action as well as global glucose homeostasis. This chapter reviews the evidence linking EDCs to diabetes risk across this spectrum of evidence. It is hoped that improving our understanding of the environmental drivers of diabetes development will illuminate novel individual-level and policy interventions to mitigate the impact of this devastating condition on vulnerable communities and the population at large.

Keywords: Bisphenol; Diabetes; Endocrine disruptor; Endocrine-disrupting chemical; Glucose; Insulin; Pesticide; Phthalate; Pollution; Polychlorinated biphenyl.

Fig. 1

Sources of environmental endocrine-disrupting chemicals. PAH: polycyclic aromatic hydrocarbon, PCB: polychlorinated biphenyl, PBDE: polybrominated diphenyl ethers.

Fig. 2

Mechanisms by which environmental endocrine-disrupting chemicals have been linked to dysfunction in metabolic tissues. Environmental EDCs may disrupt insulin signaling by damaging both insulin-releasing pancreatic beta cells (left) and insulin-responsive target tissues such as liver, adipose, and skeletal muscle (right). Created with BioRender.com.