title: The injurious effects of hyperinsulinism on blood vessels.
abstract: Insulin resistance (IR) is a common feature of hypertension, Type II diabetes, coronary heart disease, Syndrome X, and other vascular diseases. It refers to a state in which a certain concentration of insulin produces less biologic effect than expected in human body. When IR develops, the response of human body to insulin decreases accordingly, thus inducing the compensatory hyper-secretion of insulin and consequently hyperinsulinism. Many clinical and epidemiologic studies have demonstrated that IR and iatrogenic hyperinsulinism induced consequently play an essential role in the pathogenesis of hypertension and atherosclerotic cardiovascular diseases. Therefore, more and more attention should be paid to the mechanism of IR in order to explore more therapeutic basis and prospective for the treatment of atherosclerosis and other cardiovascular diseases. In this review, we provided a general overview on the known molecular mechanisms of IR and summarized the recent findings on the injurious effects of hyperinsulinism in vitro and in vivo, which might be important for researchers and clinicians to better understand the etiology and clinical significance of IR.
authors.affiliation: Department of Internal Medicine, Department of Cardiology, The 3rd Affiliated (DaPing) Hospital, The 3rd Military Medical University, Chongqing, People's Republic of China, wangxuk@163.com.
authors.forename: Xukai
authors.initials: X
authors.lastname: Wang
authors.forename: Changqing
authors.initials: C
authors.lastname: Yu
authors.forename: Bo
authors.initials: B
authors.lastname: Zhang
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
mesh_terms: D001161:Arteriosclerosis / Q000209:etiology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D006946:Hyperinsulinism / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D006973:Hypertension / Q000209:etiology; D007333:Insulin Resistance; D020929:Mitogen-Activated Protein Kinase Kinases / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000187:drug effects / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism / Q000633:toxicity; D017526:Receptor, IGF Type 1 / Q000378:metabolism
chemical_list: D009569:Nitric Oxide; D017526:Receptor, IGF Type 1; D020929:Mitogen-Activated Protein Kinase Kinases