Year: 2011
Type: article
Abstract: Diabetes mellitus is a chronic metabolic disease characterized by hyperglycemia, due to deficiency in insulin or insulin resistance, and represents a major cause of morbidity and mortality in contemporary societies [1,2].According to the world health organization (WHO), more than 285 million people worldwide suffered from diabetes of which 4 million died in 2010.The prevalence is expected to enhance to 380 million by 2030.Genetic and environmental factors associated with life style such as unhealthy diet, physical inactivity, harmful use of alcohol and tobacco, and obesity contribute to the increasing incidence of diabetes.The situation becomes extremely critical since type 1 and type 2 diabetes compromise the cardiovascular homeostasis.Based on the report of WHO and clinical studies, the direct cause of death for 80 % of diabetic patients is cardiovascular diseases.Studies in human and experimental diabetic animal models have reported vascular dysfunction and structural arterial wall remodeling [3][4][5].It is well known that endothelial dysfunction is an important risk factor of cardiovascular diseases [6,7].Several hypothesis and mechanisms documented the relationship between diabetes and microvascular endothelial dysfunction [8,9], which include reduced endothelium-derived relaxing factor (EDRF) release and bioavailability, and enhanced endothelium-derived constricting factors release associated with augmented oxidative stress levels.Despite treatments have progressed, the development of novel effective treatments for patients with vascular complications in diabetes remains a major research goal.The presence of insulin receptors on endothelial cells is well documented [10] but the role of insulin resistance at the level of the endothelial cell in vascular physiopathology is unclear.A number of studies in humans and genetically modified mice have demonstrated a close association between insulin resistance and nitric oxide (NO) bioactivity.Thus, Steinberg et al. [11] and Wheatcroft et al. [12] reported a direct link between insulin-induced vasodilatation and nitric oxide synthase (eNOS) activity.Additionally, Kuboki et al. [13] demonstrated that insulin regulates eNOS transcription in endothelial cells.Another study by Dr. Quon et al. [14] elucidated that insulin activates eNOS by insulin receptor tyrosine
Source: Journal of Diabetes & Metabolism
Authors: Modar Kassan, Maria Galán, Soo- Kyoung Choi
Institution: Tulane University
Language: English
Subfield: Cell Biology
Domain: Life Sciences
Open Access status: hybrid
OpenAlex ID: W2093332821