Abstract

BackgroundThe prevalence of hypertension and obesity has increased significantly in recent decades. Hypertension and obesity often coexist, and both are associated with increased cardiovascular mortality. Obese hypertensive patients usually require special anti-hypertensive treatment strategy due to the increased risk of treatment resistance. Molecules that can target both obesity and hypertension underlying pathologies should get more attention. Herein, we evaluated the therapeutic effects of telmisartan, with special interest in visceral adipose tissue dysfunction, in obesity-related hypertension rat model.MethodsThirty male Wistar rats weighing 150–200 g were equally divided into: 1—Control group (fed normal laboratory diet for 24 weeks), 2—Diet-induced obesity group (DIO, fed high fat diet for 24 weeks), and 3—Diet-induced obesity treated with telmisartan group (DIO + Tel, fed high fat diet and received telmisartan for 24 weeks). At the end of the study, anthropometrical parameters were evaluated. Systolic blood pressure and heart rate were measured. Blood samples were collected for the measurement of serum lipids, adipokines, cardiac, renal, inflammatory, and oxidative stress biomarkers. Kidneys were removed and used for histopathological studies, and visceral adipose tissue was utilized for histopathological, immunohistochemical and RT-PCR studies.ResultsHigh fat diet resulted in obesity-related changes in anthropometrical parameters, elevation of blood pressure, increase in heart rate, higher serum levels of cardiac, inflammatory and kidney function biomarkers, with altered serum lipids, adipokines and oxidative stress markers. Morphological changes (H&E and PAS-stained sections) were noticed in kidneys and visceral adipose tissue. Immunohistochemistry and RT-PCR studies confirmed adipose tissue dysfunction and over-expression of inflammatory and oxidative stress proteins. Telmisartan countered obesity-induced alterations in cardiovascular, renal, and adipose tissue functions.ConclusionAdipose tissue dysfunction could be the core pathophysiology of obesity-related hypertension. Besides its anti-hypertensive effect, telmisartan had profound actions on visceral adipose tissue structure and function. Attention should be given to polymodal molecules targeting adipose tissue-related disorders.

Highlights

  • The prevalence of hypertension and obesity has increased significantly in recent decades

  • Body mass index (BMI) increased significantly in the Diet induced obesity (DIO) group when compared to the control group (0.83 ± 0.03 vs 0.61 ± 0.02 g/cm2, P < 0.05)

  • The body mass index (BMI) decreased significantly in the DIO + Tel rats when compared to the DIO rats (0.71 ± 0.04 vs 0.83 ± 0.03 g/cm2, P < 0.05)

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Summary

Introduction

The prevalence of hypertension and obesity has increased significantly in recent decades. Hypertension and obesity often coexist, and both are associated with increased cardiovascular mortality. Obese hypertensive patients usually require special anti-hypertensive treatment strategy due to the increased risk of treatment resistance. We evaluated the therapeutic effects of telmisartan, with special interest in visceral adipose tissue dysfunction, in obesity-related hypertension rat model. Obesity associated comorbidities have become an increasing major health risk as well as a huge burden on health systems [1]. Hypertension and associated cardiometabolic disorders are unfavoured major outcomes of obesity or even overweight. Adipose tissue distribution has a remarkable impact; obesity associated with increased visceral adiposity is considered as a major cause of hypertension and accounts for almost three-fourth of the risk of developing essential hypertension. Adipose tissue dysfunction represents tissue remodelling characterized by adipocyte hypertrophy and hyperplasia, increased secretion of pro-inflammatory adipokine, inflammatory cell infiltration, mitochondrial dysfunction, and tissue inflammation [5, 7, 8]

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