High-Dose Treatment With Telmisartan Induces Monocytic Peroxisome Proliferator-Activated Receptor-γ Target Genes in Patients With the Metabolic Syndrome

Abstract

Abstract-The present study aimed to explore the anti-inflammatory effects and peroxisome proliferator-activated receptor-␥ (PPAR␥)-activating properties of the angiotensin type 1 receptor blocker telmisartan by analysis of serum interleukin 6 levels and monocytic PPAR␥ target gene expression in drug-naïve patients with the metabolic syndrome. This was a 14-week, randomized, double-blind, placebo-controlled 2-center study with telmisartan 80 mg/d and telmisartan 160 mg/d in 54 patients with the metabolic syndrome. In addition to clinical laboratory measurements, peripheral monocytes were extracted by negative isolation using a Dynal Monocyte kit to evaluate ligand-activated PPAR␥ target gene expression (CD36 and CD163) at baseline and study end using quantitative real-time RT-PCR. In this low-risk patient population, telmisartan (80 and 160 mg) treatment did not significantly affect serum interleukin 6 levels. Expression of the PPAR␥ target gene CD36 in monocytes was markedly induced by telmisartan from baseline to study end (telmisartan 80 mg: 2.3Ϯ1.

Evidence-based nutritional and pharmacological interventions targeting chronic low-grade inflammation in middle-age and older adults: A systematic review and meta-analysis

“…Following full text revision of remaining 289 articles, other 240 studies were excluded. Overall, 49 RCTs (Bahr et al, 2011; Bays et al, 2013; Bitzur et al, 2010; Bo et al, 2016; Breslavsky et al, 2013; Caballero et al, 2004; Chandler et al, 2014; Darghosian et al, 2015; Dawczynski et al, 2013; De Jager et al, 2005; de Jager et al, 2014; Duggan et al, 2015; Ebrahimi et al, 2009; Feher et al, 2014; Gagnon et al, 2014; Goldberg et al, 2014; Hass et al, 2014; Hutchins et al, 2013; Krysiak et al, 2011, 2013; Link et al, 2006; Magyar et al, 2012; Mazloom et al, 2013; Militaru et al, 2013; Mohamadshahi et al, 2014; Murphy et al, 2007; Nodari et al, 2011; Ogino et al, 2010; Paoli et al, 2015; Persson et al, 2006; Pooya et al, 2010; Pot et al, 2009; Pradhan et al, 2009; Rajkumar et al, 2014; Sadiya et al, 2015; Schiano et al, 2008; Shaseb et al, 2016; Sinha-Hikim et al, 2015; Sokol et al, 2012; Stricker et al, 2012; Tome-Carneiro et al, 2012; Tousoulis et al, 2008; Troseid et al, 2009; Valentini et al, 2015; van der Zijl et al, 2011; Witte et al, 2014; Xu et al, 2015; Zhao et al, 2009; Zittermann et al, 2009) were selected for the final analysis (one RCT (Rajkumar et al, 2014) was eligible among both omega −3 and probiotics). Fig.…”

“…Seven of 146 potential articles involving 528 participants met our inclusion criteria (Bahr et al, 2011; Hass et al, 2014; Link et al, 2006; Ogino et al, 2010; Persson et al, 2006; Tousoulis et al, 2008; van der Zijl et al, 2011). The included studies tested five different ARBs: losartan, valsartan, candesartan, irbesartan and telmisartan.…”

“…For example, the findings from studies testing different dosages of compounds or including different sub-studies, were extracted separately. In the article of Bahr et al (2011) we excluded results referring to treatment with telmisartan 80 mg because mean age in that group was less than 45, therefore, we considered only findings from groups under telmisartan 160 mg and placebo. All values were converted to the same units of measure: pg/ml for IL-6 and mg/L for CRP.…”

A Systematic Comparison of the Properties of Clinically Used Angiotensin II Type 1 Receptor Antagonists

“…In a small, open-label, parallel group study with losartan treatment of patients with hypertension, drug plasma levels reached values compatible with PPAR-g activation; concomitantly, PPAR-g target genes were found to be upregulated in monocytes from losartan-treated patients (Kappert et al, 2009). In a follow-up study, high doses of telmisartan (80 and 160 mg/day) in patients with metabolic syndrome also upregulated the PPAR-g target genes CD36 and CD136 in monocytes (Bähr et al, 2011). In small crossover study, overweight patients with hypertension were randomized to eprosartan versus telmisartan treatment; some metabolic parameters, which in animal studies involved PPAR-g, were significantly more improved by telmisartan than by eprosartan (Fogari et al, 2009).…”

Effect of telmisartan in hypertensive patients with impaired fasting glycaemia

“…10 The present results can also be reinforced with Bahr IN et al, high-dose treatment with telmisartan induces monocytic peroxisome proliferators-activated receptor-γ target genes in patients with the metabolic syndrome which demonstrates its role in positive actions on lipid and glucose metabolism prevention of new onset of diabetes. 12 No serious adverse effects were observed during the study period. After completion of the study period (6months), patients were advised to continue antihypertensive medication and life style changes like increasing physical activity, intake of low salt and highfibre diet.…”