Rosiglitazone influences the expression of leukocyte adhesion molecules and CD14 receptor in type 2 diabetes mellitus patients
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
24908235
DOI
10.33549/physiolres.932791
PII: 932791
Knihovny.cz E-resources
- MeSH
- Biomarkers blood MeSH
- Diabetes Mellitus, Type 2 blood drug therapy immunology MeSH
- Down-Regulation MeSH
- Hypoglycemic Agents therapeutic use MeSH
- Blood Glucose drug effects metabolism MeSH
- Middle Aged MeSH
- Humans MeSH
- Lipopolysaccharide Receptors blood MeSH
- Inflammation Mediators blood MeSH
- Cell Adhesion Molecules blood MeSH
- Rosiglitazone MeSH
- Aged MeSH
- Case-Control Studies MeSH
- Thiazolidinediones therapeutic use MeSH
- Treatment Outcome MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Biomarkers MeSH
- Hypoglycemic Agents MeSH
- Blood Glucose MeSH
- Lipopolysaccharide Receptors MeSH
- Inflammation Mediators MeSH
- Cell Adhesion Molecules MeSH
- Rosiglitazone MeSH
- Thiazolidinediones MeSH
Diabetes mellitus is associated with increased inflammatory response, which may contribute to atherosclerosis progression. Experimental results demonstrated anti-inflammatory activity of glitazones; their effect on leukocyte adhesion molecules has not been studied to date. We therefore studied the effect of rosiglitazone treatment on leukocyte surface expression of adhesion molecules in patients with type 2 diabetes mellitus and compared our results with findings in healthy subjects. 33 subjects with type 2 diabetes and 32 healthy controls were included; patients were examined at baseline and after 5 months of rosiglitazone treatment (4 mg/d). Leukocyte expression of adhesion molecules LFA-1, CD18 and ICAM-1 was quantified using flow cytometry; in addition, CD14 (lipopolysaccharide receptor) expression was analyzed as a marker of nonspecific immunity. The expression of examined molecules at baseline was higher in patients compared to controls. Despite only mild decrease in blood glucose, rosiglitazone treatment induced substantial decrease of CD18 and CD14 expression and borderline decrease of LFA-1 and ICAM-1 expression (on monocytes only). We thus observed improvement in the expression of leukocyte inflammatory markers after rosiglitazone treatment. This effect is supposed to be mediated by direct effect of rosiglitazone on PPAR-gamma receptors on leukocytes.
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