title: Relationship between insulin resistance and inflammatory markers and anti-inflammatory effect of losartan in patients with type 2 diabetes and hypertension.
abstract: BACKGROUND
  It is now well established that vascular inflammation and endothelial dysfunction associated with cardiovascular diseases contributes to insulin resistance.
  
  
  METHODS
  We investigated the relationship between the homeostasis model assessment-insulin resistance index (HOMA-R) and various serum inflammatory markers and the effect of losartan on serum concentrations of these markers in patients with type 2 diabetes and hypertension. The patients were divided into 2 groups according to the value of HOMA-R with 60 patients with values=2.4 in Group A and 44 patients with values>2.5 in Group B. The variables were measured at baseline and after 6 months of treatment with losartan (50 mg/day).
  
  
  RESULTS
  The HOMA-R concentrations were positively related to TNF-alpha (r=0.336, P<0.01) and inversely related to adiponectin (r=-0.405, P<0.01) and extracellular-superoxide dismutase (EC-SOD) (r=-0.452, P<0.01). Stepwise multiple regression analysis showed a significant relationship between HOMA-R and adiponectin (F=8.74) and EC-SOD (F=14.39). In Group B, losartan treatment significantly increased the serum concentrations of EC-SOD and adiponectin and decreased TNF-alpha and HOMA-R.
  
  
  CONCLUSIONS
  Serum EC-SOD concentrations may be a sensitive biochemical marker of insulin resistance in patients with type 2 diabetes and hypertension and that losartan improves insulin sensitivity by increasing EC-SOD and adiponectin production and decreasing TNF-alpha production.
authors.affiliation: Department of Internal Medicine, Saiseikai Suita Hospital, Osaka 564-0013, Japan.
authors.forename: Hyohun
authors.initials: H
authors.lastname: Park
authors.forename: Goji
authors.initials: G
authors.lastname: Hasegawa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Obayashi
authors.forename: Aya
authors.initials: A
authors.lastname: Fujinami
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Ohta
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Hara
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Adachi
authors.forename: Shoko
authors.initials: S
authors.lastname: Tamaki
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Nakajima
authors.forename: Fumiaki
authors.initials: F
authors.lastname: Kimura
authors.forename: Masakazu
authors.initials: M
authors.lastname: Ogata
authors.forename: Michiaki
authors.initials: M
authors.lastname: Fukui
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Yoshikawa
authors.forename: Naoto
authors.initials: N
authors.lastname: Nakamura
mesh_terms: D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D007249:Inflammation / Q000097:blood / Q000188:drug therapy*; D007333:Insulin Resistance; D019808:Losartan / Q000627:therapeutic use*; D008297:Male
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D019808:Losartan