title: Angiotensin blockade in diabetic patients decreases insulin resistance-associated low-grade inflammation.
abstract: 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.
  
  
  METHODS
  Seventeen patients with DM2 of <5years duration were recruited for the study. Patients received 4mg of candesartan, an angiotensin receptor blocker, for 6months. 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.
authors.affiliation: First Department of Pediatrics, Athens University Medical School, Athens, Greece.
authors.forename: Maria G
authors.initials: MG
authors.lastname: Pavlatou
authors.forename: George
authors.initials: G
authors.lastname: Mastorakos
authors.forename: Alexandra
authors.initials: A
authors.lastname: Margeli
authors.forename: Evangelia
authors.initials: E
authors.lastname: Kouskouni
authors.forename: Nicholas
authors.initials: N
authors.lastname: Tentolouris
authors.forename: Nikos
authors.initials: N
authors.lastname: Katsilambros
authors.forename: George P
authors.initials: GP
authors.lastname: Chrousos
authors.forename: Ioannis
authors.initials: I
authors.lastname: Papassotiriou
mesh_terms: D000328:Adult; D000368:Aged; D000804:Angiotensin II / Q000627:therapeutic use*; D057911:Angiotensin Receptor Antagonists / Q000627:therapeutic use*; D001562:Benzimidazoles / Q000627:therapeutic use*; D001713:Biphenyl Compounds; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis; D007333:Insulin Resistance / Q000502:physiology; D015850:Interleukin-6 / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D013777:Tetrazoles / Q000627:therapeutic use*; D013997:Time Factors; D016896:Treatment Outcome; D014662:Vasoconstrictor Agents / Q000627:therapeutic use*
chemical_list: D057911:Angiotensin Receptor Antagonists; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D018836:Inflammation Mediators; D015850:Interleukin-6; D013777:Tetrazoles; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; C081643:candesartan