Insulin Resistance, Diabetes & Cardiovascular Disease
Type 2 diabetes mellitus is a modern epidemic characterized by underlying insulin resistance and impaired insulin secretion. The states of impaired fasting glucose, impaired glucose tolerance and overt diabetes are associated with progressively increased risks of all-cause and cardiovascular disease (CVD)-related mortality compared with normal glucose tolerance.[2–4] Insulin resistance contributes to disordered glucose metabolism and Type 2 diabetes and may represent a risk factor for CVD independently of diabetes.[5,6] Mechanisms by which insulin resistance and Type 2 diabetes accelerate the development of atherosclerosis (which then manifests with CVD, e.g., heart attack, stroke or arterial disease) include the toxic effects of elevated glucose or glucose metabolites on the vascular endothelium, or deficiency of insulin action contributing to endothelial dysfunction, lipid abnormalities and inflammation (for reviews, see[7,8]). Treating risk factors and having a better control of glucose levels in individuals with Type 2 diabetes can over time partially reduce CVD events and mortality, but substantial residual risk remains.[9–11] Lifestyle or pharmacological interventions can reduce insulin resistance and risk of progression to Type 2 diabetes, but limited resources and drug safety concerns are barriers to providing the required intensive therapy to large numbers of people over long periods of time.[12,13] Together, diabetes and CVD represent an ever-increasing burden of morbidity and premature mortality consuming substantial healthcare resources.[14,15] Improved understanding of the pathophysiology of insulin resistance and its relationship with CVD would help to identify those at the highest risk of poorer health outcomes and provide a foundation for developing novel preventative or therapeutic approaches to preserving health.
Expert Rev Endocrinol Metab. 2011;6(2):177-185. © 2011 Expert Reviews Ltd.
Cite this: Osteocalcin: An Endocrine Link Between Bone and Glucose Metabolism - Medscape - Mar 01, 2011.