Attenuation of Endothelial Dysfunction in Diabetes Mellitus: An Integral Characteristic of Anti-Diabetic Medications

Abstract Background: The complications of diabetes mellitus (DM) have incapacitated many patients, especially in poor-income countries. DM is an endocrine disease but its far-reaching complications arise from cardiovascular derangements. The cardiovascular complications usually stem from endothelial dysfunction, which culminates in atherosclerosis. Progressively, atherosclerosis results in microvascular and macrovascular complications. Materials and Methods: Literature searches were carried out in Google, PubMed, and MEDLINE using the following keywords: DM, endothelial dysfunction, biomarkers, anti-diabetic drugs, C-reactive protein (CRP), and intercellular adhesion molecule. Original articles, systematic reviews, and meta-analytic articles were reviewed, and important findings were incorporated into this review. Summary: The review aims to evaluate mechanisms responsible for endothelial dysfunction in diabetes. Endothelial dysfunction may arise from one or a combination of these molecular mechanisms: (i) decreased nitric oxide synthesis, (ii) activation of protein kinase C and reactive oxygen species generation, (iii) activity of advanced glycation endproducts, (iv) activation of tumor necrosis factor-alpha, and (iv) defective insulin signaling and so on. The biomarkers of endothelial dysfunction were also explored and they include CRP, intracellular adhesion molecule-1, vascular cell adhesion molecule-1, microalbuminuria, asymmetric dimethylarginine, Toll-like receptors, and others. The review also evaluated the effectiveness of anti-diabetic medications in modulating the biomarkers of endothelial dysfunction in diabetic patients.