Metabolic effects of telmisartan in subjects with abdominal obesity: A prospective randomized controlled trial

Abstract

Background. Abdominal obesity, characterized by ectopic fat deposition in skeletal muscle and liver tissue, has been associated with insulin resistance and increased risk for type 2 diabetes mellitus. The aim of this study was to evaluate whether treatment with the angiotensin II type 1 (AT-1) receptor blocker telmisartan can reduce intramyocellular lipid (IMCL) and hepatic fat storage, thereby improving insulin sensitivity among individuals with abdominal obesity. Methods. Ninety-five adults with abdominal obesity (body mass index ≥ 30 kg/m² and waist circumference > 102 cm in men and > 88 cm in women) were randomized to double-blind treatment with telmisartan or placebo for 24 weeks. Following 4 weeks of 80 mg telmisartan per day, the dose was increased to 160 mg telmisartan for the duration of the study. Soleus muscle IMCL and liver fat content were assessed by ¹H-magnetic resonance imaging (¹H-MRI) spectroscopy. Secondary outcomes included changes in body composition, plasma lipids, glucose profiles, insulin sensitivity, beta-cell function and total adiponectin levels. Results. There was no significant effect of telmisartan in abdominally obese individuals consuming either a low or high glycemic diet, on IMCL content (5.73 ± 1.11 vs 6.11 ± 1.11; p = 0.13) or liver fat (0.08 ± 0.05 vs 0.09 ± 0.05; p = 0.60). Body composition, lipid and glucose profiles, insulin sensitivity and adiponectin were likewise unaffected. Beta-cell function, as determined by the insulinogenic index (IGI), improved significantly (19.3 ± 13.7 vs 22.5 ± 17.6; p = 0.03; 16.5% increase from baseline in the telmisartan group). Conclusions. Telmisartan increased beta-cell function but did not decrease IMCL or liver fat content or other metabolic parameters among individuals with abdominal obesity.

Trial registration: ClinicalTrials.gov identifier: NCT00147264.

Key Words::

• Adipokines
• adiponectin
• angiotensin receptor blockade
• ectopic fat
• glucose tolerance
• lipids
• metabolism
• obesity

Acknowledgements

We are grateful to Scott Lear and Simi Kohli, School of Kinesiology, Simon Fraser University, Burnaby, British Columbia, for assistance in the analyses of the MRI scans. The study was funded by Heart and Stroke Canada and Boehringer Ingelheim (BI), Canada (manufacturers of Telmisartan). BI were not involved in the trial design or conduct. All data were collected and analyzed by the investigators.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.