Abstract

BackgroundInformation about the renin–angiotensin–aldosterone system (RAAS) in obese individuals before and after bariatric surgery is scarce. Aim of this study was to analyze the RAAS in severely obese subjects, in relation to anthropometric and metabolic variables, with special reference to glucose tolerance.Methods239 subjects were evaluated at baseline, and 181 one year after bariatric surgery [laparoscopic gastric banding (LAGB)].ResultsAt baseline, renin (plasma renin activity, PRA) was increased from normal to glucose tolerance and more in diabetes, also correlating with ferritin. After LAGB, the decrease of PRA and aldosterone was significant in hypertensive, but not in normotensive subjects, and correlatied with decrease of ferritin. PRA and glucose levels were predictive of persistent hypertension 1 year after LAGB.ConclusionsThese data support the role of RAAS in the pathophysiology of glucose homeostasis, and in the regulation of blood pressure in obesity. Ferritin, as a proxy of subclinical inflammation, could be another factor contributing to the cross-talk between RAAS and glucose metabolism.

Highlights

  • Arterial hypertension is a major risk factor for all cardiovascular diseases (CVD), including coronary heart disease (CHD), stroke, atrial fibrillation, heart failure (HF), aortic and peripheral arterial disease, and valvular heart disease [1]

  • Triglycerides were different among the three groups; in addition, diastolic BP, ferritin were higher for type 2 diabetes (T2D) than impaired glucose tolerance (IGT) and normal glucose tolerance (NGT), and HDLcholesterol were lower; the frequency of hypertensive subjects was higher for IGT and T2D than NGT

  • Baseline supine plasma renin activity (PRA) levels were significantly correlated with age, glycemic parameters, leptin, ferritin, calcium, sodium, ALD and uric acid (Table 3)

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Summary

Introduction

Arterial hypertension is a major risk factor for all cardiovascular diseases (CVD), including coronary heart disease (CHD), stroke, atrial fibrillation, heart failure (HF), aortic and peripheral arterial disease, and valvular heart disease [1]. As the prevalence of obesity increases, its comorbidities [arterial hypertension, sleep apnea, impaired glucose tolerance (IGT) type 2 diabetes (T2D) with their associated cardiovascular (CV) risk], will increase as well. These co-morbidities are probably inter-related, due to hyperleptinemia and leptin resistance, oxidative stress, sub-clinical inflammation, endothelial dysfunction, sympathetic activation, insulin resistance (IR), and overactivation of RAAS [7]. Aim of this study was to analyze the RAAS in severely obese subjects, in relation to anthropometric and metabolic variables, with special reference to glucose tolerance

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