Purpose of review: The goal of this review is to delineate the following: (1) the primary means of inorganic arsenic (iAs) exposure for human populations, (2) the adverse public health outcomes associated with chronic iAs exposure, (3) the pathophysiological connection between arsenic and type 2 diabetes (T2D), and (4) the incipient evidence for microRNAs as candidate mechanistic links between iAs exposure and T2D.
Recent findings: Exposure to iAs in animal models has been associated with the dysfunction of several different cell types and tissues, including liver and pancreatic islets. Many microRNAs that have been identified as responsive to iAs exposure under in vitro and/or in vivo conditions have also been shown in independent studies to regulate processes that underlie T2D etiology, such as glucose-stimulated insulin secretion from pancreatic beta cells. Defects in insulin secretion could be, in part, associated with aberrant microRNA expression and activity. Additional in vivo studies need to be performed with standardized concentrations and durations of arsenic exposure in order to evaluate rigorously microRNAs as molecular drivers of iAs-associated diabetes.
Keywords: Arsenic; Diabetes; Insulin; Metabolism; MicroRNAs; β-Cell.