title: Increased serum concentrations of adhesion molecules but not of chemokines in patients with Type 2 diabetes compared with patients with Type 1 diabetes and latent autoimmune diabetes in adult age: action LADA 5.
abstract: OBJECTIVE
  Systemic concentrations of adhesion molecules and chemokines are associated with increased risk of cardiovascular complications. We compared these factors between patients with Type 2 diabetes vs. Type 1 diabetes or latent autoimmune diabetes in adults.
  
  
  METHODS
  Serum concentrations of adhesion molecules sE-selectin, sICAM-1 and sVCAM-1, and chemokines CCL2, CCL3 and CCL4 were measured in 61 patients with latent autoimmune diabetes in adults, 90 with Type 1 diabetes, 465 with Type 2 diabetes and in 41 control subjects, using multiple regression models to adjust for possible confounders.
  
  
  RESULTS
  Patients with Type 2 diabetes exhibited greater concentrations of adhesion molecules (P < 0.02) than those with Type 1 diabetes, latent autoimmune diabetes in adults and control subjects. These differences persisted upon adjustments for age, sex, BMI, blood pressure and diabetes duration (P < 0.04). Higher BMI positively correlated with concentrations of adhesion molecules in all subjects (P < 0.0001). Concentrations of sE-selectin positively related to diastolic (β = 0.31) and systolic (β = 0.28) blood pressure in the adjusted model (P < 0.04). Concentrations of the chemokines, CCL2 and CCL4, did not differ between groups, while CCL3 was higher in patients with latent autoimmune diabetes in adults and Type 1 diabetes than in those with Type 2 diabetes and control subjects (P < 0.05).
  
  
  CONCLUSIONS
  Systemic concentrations of adhesion molecules, but not chemokines, relate to cardiovascular risk factors, but remain higher after adjustments in Type 2 diabetes, suggesting a diabetes-type specific effect without difference between latent autoimmune diabetes in adults and Type 1 diabetes, despite their dissimilar phenotype.
authors.affiliation: Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany. minh.pham@ddz.uni-duesseldorf.de
authors.forename: M N
authors.initials: MN
authors.lastname: Pham
authors.forename: M I
authors.initials: MI
authors.lastname: Hawa
authors.forename: M
authors.initials: M
authors.lastname: Roden
authors.forename: G
authors.initials: G
authors.lastname: Schernthaner
authors.forename: P
authors.initials: P
authors.lastname: Pozzilli
authors.forename: R
authors.initials: R
authors.lastname: Buzzetti
authors.forename: W A
authors.initials: WA
authors.lastname: Scherbaum
authors.forename: J
authors.initials: J
authors.lastname: Seissler
authors.forename: S
authors.initials: S
authors.lastname: Hunter
authors.forename: R D G
authors.initials: RD
authors.lastname: Leslie
authors.forename: H
authors.initials: H
authors.lastname: Kolb
authors.forename: N C
authors.initials: NC
authors.lastname: Schloot
mesh_terms: D000328:Adult; D000368:Aged; D001794:Blood Pressure; D015992:Body Mass Index; D002318:Cardiovascular Diseases / Q000097:blood* / Q000276:immunology / Q000503:physiopathology; D018925:Chemokines / Q000097:blood*; D003430:Cross-Sectional Studies; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000276:immunology / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000276:immunology / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000097:blood* / Q000276:immunology / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood*
chemical_list: D018925:Chemokines; D019010:Vascular Cell Adhesion Molecule-1