Antiapoptotic and insulin-releasing effects of zinc supplementation in type-1 diabetes through ATP sensitive potassium channels

Abstract

Diabetes, which is a frequently observed disease in the overall world, is the defect of glucose metabolism due to insulin deficiency. Decreased insulin is not sufficient to transport the glucose we receive through nutrition to the cells. As part of the treatment of insulin-dependent diabetes, known as type 1 diabetes, attempts are made on recovering the pathologies developing due to the disease by performing insulin injection. Zinc is an element of trace amount in our body. Although its effects in secretion of insulin have still not been clarified thoroughly, it functions in insulin packaging and secretion particularly in beta-cells. Mechanism of action or pathways of zinc on insulin secretion still remains a mystery. Under normal circumstances, adenosine triphosphate (ATP) sensitive potassium (KATP) plays a key role in the secretion of insulin from beta-cells. It is claimed that zinc may somehow block KATP activity.