Irbesartan for the treatment of hypertension in patients with the metabolic syndrome: A sub analysis of the Treat to Target post authorization survey. Prospective observational, two armed study in 14,200 patients

Kintscher, Ulrich; Bramlage, Peter; Paar, W. Dieter; Thoenes, Martin; Unger, Thomas

doi:10.1186/1475-2840-6-12

Cited by 87 publications

(54 citation statements)

References 36 publications

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“…9 Several experimental studies further demonstrated that mice and rats treated with different ARBs show reduced weight gain. [11][12][13][14] Although telmisartan was reported to reduce the visceral fat, it did not influence body weight or body mass index either in the Ongoing Telmisartan Alone and in Combination With Ramipril Global Endpoint Trial or in the Prevention Regimen for Effectively Avoiding Second Strokes study.…”

Section: Discussionmentioning

confidence: 99%

“…2 Other than their antihypertensive effects, several clinical trials show that ARB can prevent the onset of type 2 diabetes mellitus. 3,4 Recently, clinical and experimental studies have shown that ARBs have effects on weight gain and obesity, [5][6][7][8][9][10][11][12][13][14][15] which indicate that ARB could be beneficial for the management of obesity related hypertension. Previous studies suggested that several pleiotropic effects of ARBs include upregulation of uncoupling protein (UCP) 1 and angiotensin II receptor type 1 expression, activation of peroxisome proliferator activated receptor (PPAR)-␥, increase of adiponectin, and promotion of caloric expenditure.…”

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confidence: 99%

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Telmisartan Prevents Weight Gain and Obesity Through Activation of Peroxisome Proliferator-Activated Receptor-δ–Dependent Pathways

Yang

et al. 2010

Hypertension

106

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Abstract-Telmisartan shows antihypertensive and several pleiotropic effects that interact with metabolic pathways. In the present study we tested the hypothesis that telmisartan prevents adipogenesis in vitro and weight gain in vivo through activation of peroxisome proliferator-activated receptor (PPAR)-␦-dependent pathways in several tissues. In vitro, telmisartan significantly upregulated PPAR-␦ expression in 3T3-L1 preadipocytes in a time-and dose-dependent manner. Other than enhancing PPAR-␦ expression by 68.2Ϯ17.3% and PPAR-␦ activity by 102.0Ϯ9.0%, telmisartan also upregulated PPAR-␥ expression, whereas neither candesartan nor losartan affected PPAR-␦ expression. In vivo, long-term administration of telmisartan significantly reduced visceral fat and prevented high-fat diet-induced obesity in wild-type mice and hypertensive rats but not in PPAR-␦ knockout mice. Administration of telmisartan did not influence food intake in mice. Telmisartan influenced several lipolytic and energy uncoupling related proteins (UCPs) and enhanced phosphorylated protein kinase A and hormone sensitive lipase but reduced perilipin expression and finally inhibited adipogenesis in 3T3-L1 preadipocytes. Telmisartan-associated reduction of adipogenesis in preadipocytes was significantly blocked after PPAR-␦ gene knockout. Chronic telmisartan treatment upregulated the expressions of protein kinase A, hormone-sensitive lipase, and uncoupling protein 1 but reduced perilipin expression in adipose tissue and increased uncoupling protein 2 and 3 expression in skeletal muscle in wild-type mice but not in PPAR-␦ knockout mice. We conclude that telmisartan prevents adipogenesis and weight gain through activation of PPAR-␦-dependent lipolytic pathways and energy uncoupling in several tissues. (Hypertension. 2010;55:869-879.)Key Words: peroxisome proliferator-activated receptor-␦ Ⅲ telmisartan Ⅲ obesity Ⅲ hormone sensitive lipase Ⅲ adipogenesis Ⅲ energy uncoupling A bdominal obesity, which increases cardiometabolic risks, is often associated with hypertension.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Telmisartan Prevents Weight Gain and Obesity Through Activation of Peroxisome Proliferator-Activated Receptor-δ–Dependent Pathways

Yang

et al. 2010

Hypertension

106

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“…Furthermore, angiotensin II (AngII), a potent vasoconstrictor, and other components of the RAS are present in adipose tissue (for a review, see Cassis et al, 2008). Clinical data suggest that angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) should be considered as the first line treatment for hypertension in obese patients (Masuo et al, 2001;Kintscher et al, 2007). Moreover, clinical data also suggest that ARBs improve insulin sensitivity, further demonstrating their utility in treating MetS in humans as well as in animal models of MetS.…”

Section: Models Related To the Renin-angiotensin Systemmentioning

confidence: 99%

Mouse models of the metabolic syndrome

Kennedy

Ellacott

King

et al. 2010

Disease Models &Amp; Mechanisms

233

224

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The metabolic syndrome (MetS) is characterized by obesity concomitant with other metabolic abnormalities such as hypertriglyceridemia, reduced high-density lipoprotein levels, elevated blood pressure and raised fasting glucose levels. The precise definition of MetS, the relationships of its metabolic features, and what initiates it, are debated. However, obesity is on the rise worldwide, and its association with these metabolic symptoms increases the risk for diabetes and cardiovascular disease (among many other diseases). Research needs to determine the mechanisms by which obesity and MetS increase the risk of disease. In light of this growing epidemic, it is imperative to develop animal models of MetS. These models will help determine the pathophysiological basis for MetS and how MetS increases the risk for other diseases. Among the various animal models available to study MetS, mice are the most commonly used for several reasons. First, there are several spontaneously occurring obese mouse strains that have been used for decades and that are very well characterized. Second, high-fat feeding studies require only months to induce MetS. Third, it is relatively easy to study the effects of single genes by developing transgenic or gene knockouts to determine the influence of a gene on MetS. For these reasons, this review will focus on the benefits and caveats of the most common mouse models of MetS. It is our hope that the reader will be able to use this review as a guide for the selection of mouse models for their own studies.

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“…In a subanalysis of the Treat to Target Postauthorization Study examining irbesartan to treat hypertension in patients with the metabolic syndrome, patients who were administered irbesartan exhibited a decrease in both systolic and diastolic blood pressure and a reduction in cardiovascular risk factors (decreases in serum triglycerides, fasting blood glucose, and waist circumference, and elevations in HDL cholesterol) [40]. These beneficial effects of irbesartan were more prominent in hypertensive patients with the metabolic syndrome, as compared with hypertensive patients without the metabolic syndrome.…”

Section: Ang II and Obesity-hypertensionmentioning

confidence: 99%

Local adipose tissue renin-angiotensin system

Cassis

Yiannikouris²,

Thatcher

2008

Current Science Inc

197

148

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A local renin-angiotensin system (RAS) has been proposed in adipocytes. Adipocytes are a suggested source of components of the RAS, with regulation of their production related to obesity-hypertension. Both angiotensin type 1 and 2 receptors have been localized to adipocytes. Angiotensin II has been demonstrated to regulate adipocyte growth and differentiation, lipid metabolism, and expression and release of adipokines and RAS components, and to promote oxidative stress. Differences in regional expression of RAS components in visceral versus subcutaneous adipose tissue have been suggested as a link between abdominal obesity and cardiovascular disease. Finally, several studies support antihypertensive efficacy of RAS blockade in patients with type 2 diabetes and obesity. Future studies should address the role of adipocyte-specific deficiency of RAS components to definitively determine the relevance of the adipose RAS to normal physiology and to the development of hypertension.

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Irbesartan for the treatment of hypertension in patients with the metabolic syndrome: A sub analysis of the Treat to Target post authorization survey. Prospective observational, two armed study in 14,200 patients

Cited by 87 publications

References 36 publications

Telmisartan Prevents Weight Gain and Obesity Through Activation of Peroxisome Proliferator-Activated Receptor-δ–Dependent Pathways

Telmisartan Prevents Weight Gain and Obesity Through Activation of Peroxisome Proliferator-Activated Receptor-δ–Dependent Pathways

Mouse models of the metabolic syndrome

Local adipose tissue renin-angiotensin system

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