Essay --

Introduction Cardiovascular disease (CVD) and chronic kidney disease (CKD) closely parallel the obesity and insulin resistance epidemic. Current U.S. estimates project 70 million obese adults and an additional 70 million with hypertension and/or type II diabetes (28, 42, 45). More so, the National Health and Nutrition Examination Survey (NHANES), suggest a graded and continuous relationship exists between prevalent hypertension and increasing body mass index (BMI); a metric that is closely associated with insulin resistance and self-identified type II diabetes (8, 34). Latent diabetic vascular complications are a hallmark of the disease and known to significantly affect the cardiovascular and renal systems. Atherosclerosis is the main reason for decreased life expectancy in patients with diabetes, whereas diabetic nephropathy and retinopathy are the largest contributors to end-stage renal disease and blindness, respectively (37, 56). Current therapy is aimed at managing blood glucose concentrations and increasing insulin resistance. Thus, vascular complication mitigation includes: blood glucose monitoring and lowering, which decreases the risk of nephropathy and retinopathy. Antihypertensive medicine is also utilized to decrease the risk of cardiovascular disease, nephropathy, and retinopathy (15, 26). As well, hypertension is closely associated with stroke and pulmonary edema. Despite these advances, diabetes complications and their treatments are aimed at abating symptoms in an effort to improve physiological function. Atherosclerosis in Diabetes Atherosclerotic lesions in patients with diabetes are indistinguishable from lesions in patients in whom another characteristic, like hypercholesterolemia or smoking, is the major ... ...hole-body insulin resistance in skeletal muscles (11, 32, 43). It should not be discounted though that the MR also has a high affinity for both aldosterone and 11ÃŽ ²-hydroxy-glucocorticoids, which exist in lower levels in non-epithelial tissues that allow glucocorticoids to signal through the MR in cardiovascular and metabolic tissue such as skeletal muscle, liver and fat (72). Not a marginal point as insulin resistant populations have plasma glucocorticoid concentrations are greater than those of aldosterone and this may promote MR activation by glucocorticoids. Potentiating the oxidative stress in the cardio-renal metabolic syndrome (71). Indepdent of the in-/direct mechanism, the evidence of RAAS blockade or silencing can ameliorate oxidative stress, improves endothelial function and contributes to reductions of hypertension in the cardio-renal metabolic phenotype.