Insulin resistance is a complex metabolic defect that has several causes dependent on an individual's genetic substrate and the underlying pathophysiologic state. Atherogenic dyslipidemia, hyperinsulinemia, dysglycemia, inflammation associated with obesity, and ectopic steatosis in liver and skeletal muscle all collude to facilitate endothelial dysfunction and predispose to the initiation and propagation of atherosclerosis. As aggressive management of the various risk factors does not seem to abrogate the so-called residual risk, more research is needed to define ways by which intervention can fundamentally alter the metabolic and vascular milieu and slow the pace of atherosclerosis, thus favorably affecting outcomes.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.hfc.2012.06.014 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!