Key result
Telmisartan significantly reduced visceral fat area compared to control therapy (weighted mean difference -18.13 cm2; 95% CI -27.16 to -9.11) in hypertensive patients with metabolic risk factors.
Why the study?
Does telmisartan improve fat distribution and reduce visceral adipose tissue in hypertensive patients with overweight/obesity, metabolic syndrome, or glucose intolerance?
Meta-Analysis
Does telmisartan improve fat distribution and reduce visceral adipose tissue in hypertensive patients with overweight/obesity, metabolic syndrome, or glucose intolerance?
Mean Difference: -18.13 (95% CI -27.16–-9.11)
Telmisartan significantly reduces visceral fat area in hypertensive patients with obesity, metabolic syndrome, or glucose intolerance compared to control therapy.
Supports telmisartan in hypertensive patients with metabolic risks; confirms visceral fat reduction in Level 1 meta-analysis.
OBJECTIVES: Several meta-analyses have confirmed the positive metabolic effects of telmisartan, an angiotensin II receptor blocker that can also act as a partial peroxisome proliferator-activated receptor-γ agonist, compared to those of other angiotensin II receptor blockers. These effects include decreased fasting glucose, glycosylated hemoglobin, interleukin-6, and tumor necrosis factor-α levels. However, no systemic analysis of telmisartan's effects on body fat distribution has been performed. We performed a meta-analysis of randomized controlled telmisartan trials to investigate its effects on body weight, fat distribution, and visceral adipose reduction. RESEARCH DESIGN AND METHODS: A literature search was performed using Embase, MEDLINE, and the Cochrane Library between January 1966 and November 2013. Randomized controlled trials in English and meeting the following criterion were included: random assignment of hypertensive participants with overweight/obesity, metabolic syndrome, or glucose intolerance to telmisartan or control therapy group. RESULTS: Of 651 potentially relevant reports, 15 satisfied the inclusion criterion. While visceral fat area was significantly lower in the telmisartan group than in the control group (weighted mean difference = -18.13 cm(2), 95% C.I. = -27.16 to -9.11, Pχ(2) = 0.19, I(2) = 41%), subcutaneous fat area was similar (weighted mean difference =2.94 cm(2), 95% C.I. = -13.01 to 18.89, Pχ(2) = 0.30, I(2) = 17%). Total cholesterol levels were significantly different between the groups (standardized mean difference = -0.24, 95% C.I. = -0.45 to -0.03, Pχ(2) = 0.0002, I(2) = 67%). LIMITATIONS: Limitations include: (1) limited number of studies, especially those evaluating fat distribution; (2) different imaging modalities to assess visceral fat area (V.F.A.) and subcutaneous fat area (S.F.A.); (3) observed heterogeneity. CONCLUSION: The findings suggest that telmisartan affected fat distribution, inducing visceral fat reduction, and thus could be useful in hypertensive patients with obesity/overweight, metabolic syndrome, or glucose intolerance.
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Choi et al. (2016) conducted a meta-analysis in Hypertension with overweight/obesity, metabolic syndrome, or glucose intolerance. Telmisartan vs. Control therapy was evaluated on Visceral fat area (WMD -18.13, 95% CI -27.16 to -9.11). Telmisartan significantly reduced visceral fat area compared to control therapy (weighted mean difference -18.13 cm2; 95% CI -27.16 to -9.11) in hypertensive patients with metabolic risk factors.
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