Treatment of Obesity Hypertension and Diabetes Syndrome

Abstract

Abstract-Obesity has been shown to be an independent risk factor for coronary heart disease. The insulin resistance associated with obesity contributes to the development of other cardiovascular risk factors, including dyslipidemia, hypertension, and type 2 diabetes. The coexistence of hypertension and diabetes increases the risk for macrovascular and microvascular complications, thus predisposing patients to cardiac death, congestive heart failure, coronary heart disease, cerebral and peripheral vascular diseases, nephropathy, and retinopathy. Body weight reduction increases insulin sensitivity and improves both blood glucose and blood pressure control. Metformin therapy also improves insulin sensitivity and has been associated with decreases in cardiovascular events in obese diabetic patients. Antihypertensive treatment in diabetics decreases cardiovascular mortality and slows the decline in glomerular function. However, pharmacological treatment should take into account the effects of the antihypertensive agents on insulin sensitivity and lipid profile. Diuretics and ␤-blockers are reported to reduce insulin sensitivity and increase triglyceride levels, whereas calcium channel blockers are metabolically neutral and ACE inhibitors increase insulin sensitivity. For the high-risk hypertensive diabetic patients, ACE inhibition has proven to confer additional renal and vascular protection. Because hypertension and glycemic control are very important determinants of cardiovascular outcome in obese diabetic hypertensive patients, weight reduction, physical exercise, and a combination of antihypertensive and insulin sensitizers agents are strongly recommended to achieve target blood pressure and glucose levels.

The effect of lowering blood pressure by magnesium supplementation in diabetic hypertensive adults with low serum magnesium levels: a randomized, double-blind, placebo-controlled clinical trial

“…Because the occurrence of diabetes and hypertension are multiplicative risk factors for macro-and microvascular disease and determinants of cardiovascular outcomes, 42 the tight control of BP and glycemia in diabetic hypertensive patients is strongly recommended for preventing cardiovascular events. 43 In clinical practice, it is almost impossible to control the BP in diabetic patients without the use of diuretics.…”

Treating hypertension while protecting the vulnerable islet in the cardiometabolic syndrome

“…Antioxidant effects include inhibition of Ang II-and aldosteroneinduced superoxide formation [120,121], improvement in NO bioavailability [120,121], and reduction of oxidative stress [122,123]. CCBs have minimal effects on lipid levels [117,118,124,125].…”

“…ACE inhibitors may prevent or reduce Ang II-mediated interference with insulin-signaling pathways, evidenced by increased glucose transporter-4 protein content in skeletal muscle [147]. They may improve lipid levels by improving carbohydrate metabolism [125]. Their antioxidant effects include suppression of Ang II-induced superoxide formation [120,121] and reduction in oxidative stress [148,149].…”

Angiotensin II Type-1 Receptor Blocker Valsartan Enhances Insulin Sensitivity in Skeletal Muscles of Diabetic Mice

“…Insulin resistance occurs in a wide variety of pathological states and is commonly associated with obesity, type 2 diabetes, accelerated atherosclerosis, and hypertension. 1,2 Shimamoto et al demonstrated that the insulin sensitivity of fructose-fed rats is improved by treatment with an Ang II receptor blocker (ARB), olmesartan, caused by changes in muscle fiber composition and a decrease in tumor necrosis factor (TNF)-␣ expression in skeletal muscle. 3,4 Henriksen et al 5 reported that an ARB, irbesartan, either acutely or chronically, improves glucose tolerance in the obese Zucker rat, at least in part through enhancement of skeletal muscle glucose transport, and the effect of chronic Ang II receptor antagonism on skeletal muscle glucose uptake is associated with an increase in GLUT4 protein expression.…”