Review of diabetes: Identification of markers for early detection, glycemic control, and monitoring clinical complications

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Abstract
The hallmark of diabetes mellitus, whether type I or type II, is hyperglycemia. Clinical complications associated with diabetes are most likely the consequence of hyperglycemia via both altered metabolic pathways and nonenzymatic glycation of proteins. The nonenzymatic glycation of proteins is accelerated in diabetes due to elevated blood glucose concentration. The Amadori product of nonenzymatic glycation will further crosslink with other proteins to form advanced glycosylation end products (AGEs). The reaction of AGEs with long‐lived proteins, such as collagen, and the uptake of AGEs by the receptors on macrophages, endothelial cells, and platelets are major reasons for the development of various clinical complications in diabetes. Several markers have been identified for the screening, diagnosis, and monitoring of the disease. Autoantibodies against beta cells are the best markers for mass screening and for early detection of type I diabetes. In addition to glycated hemoglobin, AGEs and blood glycated proteins of various half‐lives could be used for monitoring glycemic control. Several abnormal metabolites have been identified as potential markers for monitoring the severity of various clinical complications. The most interesting findings in diabetic markers could be AGEs. The amount of AGEs found in the tissues could be related to the extent of micro‐ and macrovascular damage and might prove useful for monitoring the treatment of patients at early stages of either nephropathy, atherosclerosis, retinopathy, or neuropathy.