Metabolic and vascular abnormalities in subjects at risk for type 2 diabetes: the early start of a dangerous situation.
Various groups at risk for type 2 diabetes have been identified, including individuals with family history of type 2 diabetes, obesity, prior gestational diabetes, polycystic ovary syndrome, metabolic syndrome, hypertension, dyslipidemia and particularly those with pre-diabetes (impaired glucose tolerance and/or impaired fasting glucose). To various degrees, all these groups have also been identified with significant vascular abnormalities that range from endothelial dysfunction and low-grade or sub-clinical inflammation to evident atherosclerosis. The mechanisms involved in establishing a link between the risk of type 2 diabetes and vascular dysfunction are multiple and complex. The presence in the circulation of various cytokines, hormones and substrates associated with increased visceral fat and insulin resistance, the frequent appearance of associated cardiovascular risk factors and/or the possibility of some genetically determined intrinsic vascular abnormalities are all explanatory mechanisms that are being evaluated in clinical research. Whereas the possibility of appreciating a significant reduction in cardiovascular outcomes in long-term prospective clinical trials in all these groups at risk for type 2 diabetes is still lacking, understanding these mechanisms and recognizing how various interventions may improve vascular health is a worthwhile area of research that may translate into important clinical strategies to reduce the burden of type 2 diabetes and cardiovascular disease.
Caballero
A Enrique
AE
Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA. enrique.caballero@joslin.harvard.edu
D001161:Arteriosclerosis / Q000473:pathology; D002318:Cardiovascular Diseases / Q000150:complications; D002319:Cardiovascular System; D002986:Clinical Trials as Topic; D016207:Cytokines / Q000378:metabolism; D003920:Diabetes Mellitus / Q000473:pathology; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000378:metabolism* / Q000473:pathology*; D016640:Diabetes, Gestational / Q000150:complications; D004730:Endothelium, Vascular / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007249:Inflammation; D007333:Insulin Resistance; D008297:Male; D008954:Models, Biological; D009765:Obesity / Q000150:complications; D011085:Polycystic Ovary Syndrome / Q000150:complications; D011247:Pregnancy; D012306:Risk; D012307:Risk Factors
D016207:Cytokines; D005947:Glucose