|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Centre Hospitalier Universitaire Vaudois and University of Lausanne, Division of Nephrology and Department of Medicine, Lausanne, Switzerland
2 Institute of Physiology, University of Fribourg, Fribourg, Switzerland
3 Lausanne, Switzerland; Centre Hospitalier Universitaire Vaudois and University of Lausanne, Division of Nephrology and Department of Medicine, Lausanne, Switzerland
* To whom correspondence should be addressed. E-mail: azanchidel{at}hotmail.com.
Aims/Hypothesis: Glitazones are PPAR-
agonists with powerful insulin-sensitizing properties. They promote the development of metabolically active adipocytes which can lead to a substantial gain in fat mass. Telmisartan is an angiotensin II type 1 receptor antagonist with partial PPAR-
agonistic properties. Recently, telmisartan has been reported to prevent weight gain and improve insulin sensitivity in diet-induced obese rodents. The goal of this study was to examine the influence of telmisartan on pioglitazone induced weight gain and insulin sensitizing properties in two models of insulin resistance: a non genetic model (high fat fed Sprague Dawley rats) and the genetically obese fa/fa Zucker rat. Methods/Results: After a 4 week treatment, pioglitazone-induced increase in fat mass was modest in the Sprague Dawley rats and severe in the Zucker rats. In both models, these effects were substantially decreased by concomitant treatment with telmisartan. The effects of telmisartan on body weight and fat mass in the Zucker rats were abolished by pair-feeding suggesting that it is due to a decrease in food intake. Telmisartan did not interfere with the insulin-sensitizing properties of pioglitazone. Conclusions: This study demonstrates that telmisartan attenuates the glitazone-induced increase in fat mass without interfering with its insulin-sensitizing properties.
This article has been cited by other articles:
![]() |
J. C. Russell, S. D. Proctor, S. E. Kelly, and D. N. Brindley Pair feeding-mediated changes in metabolism: stress response and pathophysiology in insulin-resistant, atherosclerosis-prone JCR:LA-cp rats Am J Physiol Endocrinol Metab, June 1, 2008; 294(6): E1078 - E1087. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |