This Article Full Text Full Text (PDF) All Versions of this Article: 47/5/822    most recent 01.HYP.0000215184.00915.62v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sharma, A. M. Search for Related Content PubMed PubMed Citation Articles by Sharma, A. M. Related Collections Obesity ACE/Angiotension receptors Energy metabolism Glucose intolerance Related Article

(Hypertension. 2006;47:822.)
© 2006 American Heart Association, Inc.

Editorial Commentaries

Telmisartan

The ACE of ARBs?

Arya M. Sharma

From the Michael G. deGroote of Medicine, McMaster University, Hamilton General Hospital, Hamilton, Ontario, Canada.

Correspondence to Arya M. Sharma, McMaster University, Hamilton General Hospital, 237 Barton St East, Hamilton, Ontario, Canada, L8L 2X2. E-mail sharma@ccc.mcmaster.ca

An extract of the first 250 words of the full text is provided, because this article has no abstract.

In 2002, my colleagues and I¹ suggested that blockade of the renin-angiotensin system may prevent diabetes by promoting adipogenesis, thereby allowing redistribution of fat from dangerous visceral and ectopic fat deposits to less-dangerous subcutaneous depots. This hypothesis was based on our observation that angiotensin II inhibits human preadipocyte differentiation.² We subsequently demonstrated increased activity of the renin-angiotensin system in obesity³ and suggested, therefore, that renin-angiotensin blockade should be the treatment of choice in obesity-related hypertension.⁴

In 2004, Benson et al⁵ reported the novel observation that the highly lipophilic angiotensin receptor blocker (ARB) telmisartan may directly stimulate the peroxisome proliferator activated receptor (PPAR), a key inducer of adipocyte differentiation. Although this property has since been also reported for irbesartan⁶ and a losartan metabolite,⁷ there is no doubt that telmisartan by 1 order of magnitude is the most powerful stimulator of PPAR activity among the ARBs. Because thiazolidinediones, a class of even more potent PPAR agonists ("glitazones"), are widely used as insulin sensitizers in the treatment of type 2 diabetes mellitus and promote both adipocyte proliferation and fat redistribution, the report that telmisartan may have similar glitazone-like properties led to widespread and enthusiastic speculations regarding the possible metabolic benefits of this compound.⁸ Without doubt, such a "eumetabolic" property of an antihypertensive drug would be of considerable interest, given that the majority of patients with hypertension also have other features of the metabolic syndrome. including abdominal adiposity, dyslipidemia. and insulin resistance.

In this issue of Hypertension, Sugimoto et al⁹ provide further . . . [Full Text of this Article]

Related Article:

Telmisartan But Not Valsartan Increases Caloric Expenditure and Protects Against Weight Gain and Hepatic Steatosis

Ken Sugimoto, Nathan R. Qi, Ludmila Kazdová, Michal Pravenec, Toshio Ogihara, and Theodore W. Kurtz
Hypertension 2006 47: 1003-1009. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				A. Remuzzi and G. Remuzzi Review: Potential protective effects of telmisartan on renal function deterioration Journal of Renin-Angiotensin-Aldosterone System, December 1, 2006; 7(4): 185 - 191. [Abstract] [PDF]