Hyperglycemia Induced Osmotic Disequilibrium, Oxidative Stress and Cell Death in Type II Diabetes Patients

High unutilized glucose in the body in diabetes along with increased level of Na+ and urea cause altered osmotic equilibrium in the vascular bed contributing altered cellular microenvironment which may further affect membrane function. As plasma membrane is a dynamic structure, it is responsive to chemical exposure. Any chemical exposure may trigger alteration in membrane function and subsequently down-hill reactions. We are therefore studying the role of high glucose concentration in membrane alteration, altered cellular function and cell death in diabetic patients. In our present study we have recruited newly diagnosed 30 type II diabetes mellitus patients, chosen from diabetic clinic, Howrah Zila Hospital, Howrah, West Bengal and 31 age and sex matched healthy control without any history of diabetes from same socio economic background. Significantly high glycemic index (studied by serum glucose level and glycated haemoglobin level), high blood osmolality, osmotic fragility and oxidative stress have been noted in every diabetic participant in comparison to non-diabetic individual of our study population. A significant cell membrane alteration (p<0.05) with altered serum free sialic acid concentration has been noted in diabetic patients. Degree of membrane deformity, frequency of nonviable WBC, frequency of apoptotic cells and length of comet tail all are significantly higher (p<0.01) in diabetic persons in comparison to normal non-diabetic counterpart of the population. Diabetes is an altered homeostatic state which contributes to cellular disintegrity and cell death and is associated with osmotic dis-equilibrium.