Biorhythmic and receptor mediated interplay between melatonin and insulin: its consequences on diabetic erythrocytes

Abstract

Diabetes mellitus, one of the crucial epidemics of this country has snatched the sleep of mankind with a steep slope of 108 million in 1980 to more than 460 million in today’s world. The global statistics based on numerological information from World Health Organization (WHO) proposed alarmingly about 642 million affected individuals by 2040. Type 1 diabetes is due to damaged pancreatic β-cells while type 2 diabetes is a result of insulin insensitivity associated with hyperglycaemia. Hyperglycaemia is a principal symptom of diabetes. As a result, the circulatory erythrocytes [red blood cells (RBCs)] become the first and most vulnerable victims to confront such a stressful environment. The RBCs possess many components including haemoglobin, membrane proteins and lipids. They prefer to interact with glucose and form glycated haemoglobin and membrane phospholipid asymmetry which alters RBC adherence. These alterations trigger intracellular reactive oxygen species (ROS) formation and oxidative damage in diabetic erythrocytes. Melatonin, an indoleamine, ameliorates oxidative stress in various tissues and has the capacity of shielding erythrocytes from deleterious stress. A crucial relationship between melatonin and insulin indicates their interplay in occurrence of diabetes. Biorhythm entrained and receptor mediated action of melatonin on pancreatic β-cells in the context of hyperglycaemia are discussed for the first time in the review. Since melatonin protects against erythrocytes, as well as beneficial to diabetes, it is worthy to address proficiency of this indoleamine to the diabetic erythrocytes. In summary, this review has discussed the fostering role of melatonin in hyperglycaemia and encouraged further investigation related to the molecular pathways of melatonin on glucose metabolism.