title: Insulin resistance and adiposity correlate with acute-phase reaction and soluble cell adhesion molecules in type 2 diabetes.
abstract: OBJECTIVE
  To investigate the relationship of inflammation and endothelial activation with insulin resistance and adiposity in type 2 diabetes.
  
  
  RESULTS
  Hundred and thirty-four (45 female) type 2 diabetic subjects aged 50-75 in the Fenofibrate Intervention and Event Lowering in Diabetes Study in Helsinki were examined before fenofibrate intervention. Fasting levels of circulating intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) (vascular cell adhesion molecule), ultra-sensitive C-reactive protein (CRP), human serum amyloid A (hSAA), interleukin-6 (IL-6), macrophage colony-stimulating factor (M-CSF), secretory phospholipase A(2) IIA (PLA(2)), total, HDL and LDL cholesterol, triglycerides, P-glucose, HbA1c, and serum free insulin were determined. Insulin resistance was assessed by the homeostasis model. HOMA IR correlated significantly with all measures of adiposity and markers of inflammation and endothelial dysfunction. BMI was significantly associated with inflammation and endothelial activation, but with neither lipoproteins nor glycaemic control. After controlling for age, gender and BMI, HbA1c correlated significantly with CRP, hSAA, ICAM-1, E-selectin, and HOMA IR. HDL cholesterol correlated inversely with IL-6, M-CSF, E-selectin, and HOMA IR. HbA1c, phospholipase A(2), VCAM-1, and HDL cholesterol remained independent determinants of HOMA IR in the linear regression analysis controlled for age, gender, and BMI.
  
  
  CONCLUSIONS
  Endothelial activation and acute-phase reaction correlate with insulin resistance and obesity in type 2 diabetic patients.
authors.affiliation: Department of Internal Medicine, Helsinki University Central Hospital, Biomedicum, Haartmaninkatu 8, P.O. Box 700, 00029 HUS Helsinki, Finland. leinoee@netscape.net
authors.forename: Eeva
authors.initials: E
authors.lastname: Leinonen
authors.forename: Eva
authors.initials: E
authors.lastname: Hurt-Camejo
authors.forename: Olov
authors.initials: O
authors.lastname: Wiklund
authors.forename: Lillemor Mattson
authors.initials: LM
authors.lastname: Hultén
authors.forename: Anne
authors.initials: A
authors.lastname: Hiukka
authors.forename: Marja-Riitta
authors.initials: MR
authors.lastname: Taskinen
mesh_terms: D000210:Acute-Phase Reaction; D017677:Age Distribution; D000368:Aged; D000704:Analysis of Variance; D015415:Biomarkers / Q000032:analysis; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis / Q000378:metabolism*; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000453:epidemiology / Q000209:etiology*; D003924:Diabetes Mellitus, Type 2 / Q000175:diagnosis / Q000188:drug therapy* / Q000453:epidemiology / Q000209:etiology*; D005260:Female; D011345:Fenofibrate / Q000627:therapeutic use*; D006801:Humans; D015994:Incidence; D007333:Insulin Resistance; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000378:metabolism; D016014:Linear Models; D016173:Macrophage Colony-Stimulating Factor / Q000032:analysis / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000175:diagnosis* / Q000453:epidemiology; D010741:Phospholipases A / Q000032:analysis / Q000378:metabolism*; D011379:Prognosis; D012307:Risk Factors; D012680:Sensitivity and Specificity; D017678:Sex Distribution; D012995:Solubility; D013548:Sweden; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis / Q000378:metabolism
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D015815:Cell Adhesion Molecules; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D016173:Macrophage Colony-Stimulating Factor; D002097:C-Reactive Protein; D010741:Phospholipases A; D011345:Fenofibrate