Statin-Induced Insulin Resistance Through Inflammasome Activation: Sailing Between Scylla and Charybdis

摘要

Elevated LDL cholesterol is an independent risk factor for cardiovascular disease (CVD), and current clinical guidelines recommend aggressive reduction as the preferred course of treatment (1). Type 2 diabetes (T2D) also is a major and independent risk factor for development of CVD (2). A plethora of clinical data exists substantiating the beneficial effects of treatment with inhibitors of 3-hydroxy-3-rnethylglutaryl-CoA (HMG-CoA) reductases-commonly known as statins-on cardiovascular morbidity and mortality in both nondiabetic people and those with T2D (3). While statin therapy clearly reduces cardiovascular events, accumulating evidence indicates that statins also may confer increased risk for T2D (4). Recent analyses of both clinical trials and population-based cohort studies suggest that the cardiovascular benefits of statin therapy outweigh the risk of developing T2D (5,6). Nevertheless, findings that suggest increased incidence of T2D in some high-risk patients (e.g., those with elevated fasting glucose [5]) or in certain populations (e.g., postmenopausal women [7]) may call for greater caution in statin use, particularly at a time when its over-the-counter availability is being considered (8).