The Effects of Arsenic and Selenium on Pancreatic Beta-Cell Function

Type 2 diabetes mellitus (T2DM) is a complex metabolic disorder characterized by high blood glucose levels due to inadequate insulin secretion from pancreatic β-cell dysfunction. Conventionally accepted risk factors, such as genetics and lifestyle choices, do not account for the rapidly growing rate at which T2DM affects individuals on a global scale. Environmental exposures and their association with disease is a growing area that is elucidating associations, such as arsenic and diabetes. This study aimed to investigate how selenium and selenoprotein status affect arsenic-induced β-cell dysfunction and potentiate the development of T2DM. We observed in our study that arsenic induces β-cell dysfunction in MIN6-K8 cells, arsenic induces upregulation of selenoprotein gene expression not looked at and that the upregulated selenoproteins do not alter β-cell function. Co-treatment of selenium and arsenic showed varying results, which speaks to the complexity of how these elements are routed in the system. Selenium is known to bind to arsenic as a detoxifier, however, too much selenium is also known to exacerbate arsenic’s injurious effects. Both outcomes were observed in the co-treatment experiments and need further investigation to comprehend the interactions.