Type 2 Diabetes Mellitus and Cardiovascular Disease: Unraveling the Complex Interplay (Part II of II)

In the setting of peripheral insulin resistance (IR) characteristic of diabetes, vascular dysfunction and atherosclerotic lesions result from the loss of insulin signaling in the endothelium [1].Some authors have suggested that the implementation of pharmacological strategies that allow the control of endothelial changes can block vascular inflammation and oxidative stress (OS) and thus prevent metabolic disorders.This action may guarantee the physiological release of oxide nitric acid (NO) and capillary reorganization, as well as greater delivery and better tissue insulin sensitivity, improving the evolution of the disease and reducing the impact or appearance of complications, such as the cardiovascular [2][3][4].This is so because the role of genetic alterations induced by factors of a highly varied nature, such as the NF-kB transcription factor in OS, vascular dysfunction, inflammation, and even reduced glucose uptake by some tissues, is shown to be determinants and, therefore, axial in deciding the type of intervention in type 2 diabetes mellitus (T2DM) [5,6].