Angiotensin blockade in diabetic patients decreases insulin resistance-associated low-grade inflammation
Version of Record online: 22 DEC 2010
© 2010 The Authors. European Journal of Clinical Investigation © 2010 Stichting European Society for Clinical Investigation Journal Foundation
European Journal of Clinical Investigation
Volume 41, Issue 6, pages 652–658, June 2011
How to Cite
Pavlatou, M. G., Mastorakos, G., Margeli, A., Kouskouni, E., Tentolouris, N., Katsilambros, N., Chrousos, G. P. and Papassotiriou, I. (2011), Angiotensin blockade in diabetic patients decreases insulin resistance-associated low-grade inflammation. European Journal of Clinical Investigation, 41: 652–658. doi: 10.1111/j.1365-2362.2010.02453.x
- Issue online: 3 MAY 2011
- Version of Record online: 22 DEC 2010
- Received 8 February 2010; accepted 28 November 2010
- Angiotensin II;
- angiotensin receptor blockers;
- diabetes mellitus type 2;
- insulin resistance;
Eur J Clin Invest 2011; 41 (6): 652–658
Background Insulin-resistant states, such as metabolic syndrome and diabetes mellitus type 2 (DM2), have been associated with chronic low-grade systemic inflammation. Elevated levels of interleukin-6 (IL-6), monocyte chemoattractant protein (MCP-1) and C-reactive protein (hs-CRP), are found in patients with type 2 diabetes with and without complications. Angiotensin II (Ang II), a potent vasopressor, seems to regulate also the expression of the above inflammatory mediators acting as proinflammatory cytokine. In this study, we examined the effects of candesartan, an angiotensin receptror blocker, in the chronic low-grade inflammation observed in DM 2.
Materials and methods Seventeen patients with DM2 of < 5 years duration were recruited for the study. Patients received 4 mg of candesartan, an angiotensin receptor blocker, for 6 months. Blood levels of IL-6, MCP-1, hs-CRP and other inflammatory indices were measured before and at the end of candesartan administration.
Results At the end of treatment with candesartan, IL-6 levels decreased significantly (P < 0·05). Serum levels of MCP-1 and hs-CRP showed a trend for significant decrease with treatment (P < 0·08 and P < 0·09, respectively). Statistically significant correlations were found between hs-CRP and MCP-1 (r = 0·623, P < 0·05), IL-6 and MCP-1 (r = 0·703, P < 0·05) and TRT and MCP-1 (r = 0·752, P < 0·05), before but not at the end of candesartan administration.
Conclusions Candesartan could decrease the low-grade inflammation of type 2 DM as shown by the decrease of inflammatory mediators. Thus, angiotensin receptor blockers could be useful for treating patients with DM2 not only for their antihypertensive capacity but also for their anti-inflammatory actions.