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

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.

Dietary Selenium Deficiency Partially Mimics the Metabolic Effects of Arsenic.

Chronic arsenic exposure via drinking water is associated with diabetes in human pop-ulations throughout the world. Arsenic is believed to exert its diabetogenic effects via multiple mechanisms, including alterations to insulin secretion and insulin sensitivity. In the past, acute arsenicosis has been thought to be partially treatable with selenium supplementation, though a potential interaction between selenium and arsenic had not been evaluated under longer-term exposure models. The purpose of the present study was to explore whether selenium status may augment arsenic's effects during chronic arsenic exposure. To test this possibility, mice were exposed to arsenic in their drinking water and provided ad libitum access to either a diet replete with selenium (Control) or deficient in selenium (SelD). Arsenic significantly improved glucose tolerance and decreased insulin secretion and ß-cell function in vivo. Dietary selenium deficiency resulted in similar effects on glucose tolerance and insulin secretion, with significant interactions between arsenic and dietary conditions in select insulin-related parameters. The findings of this study highlight the complexity of arsenic's metabolic effects and suggest that selenium deficiency may interact with arsenic exposure on ß-cell-related physiological parameters.