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Countering adipose tissue dysfunction could underlie the superiority of telmisartan in the treatment of obesity-related hypertension.

Cardiovascular diabetology
January 1, 1970
Yahya M Naguib et al. (5 authors)
Journal ArticleAnimal Study
Extracted Claims (9)
InterventionDirectionEndpointPopulationDosageImpactClaim #
high fat diet
increase
obesity-related changes in anthropometrical parameters
male Wistar rats
-
resulted in
#1
high fat diet
increase
blood pressure
male Wistar rats
-
resulted in elevation of
#2
high fat diet
increase
heart rate
male Wistar rats
-
resulted in increase in
#3
high fat diet
increase
cardiac, inflammatory and kidney function biomarkers
male Wistar rats
-
resulted in higher serum levels of
#4
high fat diet
neutral
serum lipids, adipokines and oxidative stress markers
male Wistar rats
-
resulted in altered
#5
high fat diet
neutral
morphological changes in kidneys and visceral adipose tissue
male Wistar rats
-
resulted in
#6
high fat diet
increase
adipose tissue dysfunction and over-expression of inflammatory and oxidative stress proteins
male Wistar rats
-
confirmed
#7
telmisartan
decrease
obesity-induced alterations in cardiovascular, renal, and adipose tissue functions
male Wistar rats
-
countered
#8
telmisartan
neutral
visceral adipose tissue structure and function
male Wistar rats
-
had profound actions on
#9
Abstract

BACKGROUND: 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. 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. METHODS: Thirty 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. RESULTS: High 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. CONCLUSION: Adipose 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.

Medical Subject Headings (MeSH)
AdiposityAngiotensin II Type 1 Receptor BlockersAnimalsAntihypertensive AgentsBiomarkersBlood PressureDisease Models, AnimalHypertensionIntra-Abdominal FatKidneyMaleObesityRats, WistarTelmisartanRats
Study Links
PubMed ID33761942
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