Background: Activation of leukocytes is obligatory for
adherence to the endothelium and atherogenesis. Since
leukocyte activation by triglycerides (TG) and glucose has been described <i>in vitro</i>, we hypothesised higher leukocyte activation in patients with type 2 diabetes.
Methods: Using flow cytometry, we studied the expression of the leukocyte activation markers CD11A, CD11B, CD62L and CD66B in 15 patients with type 2 diabetes without clinical evidence of atherosclerosis (55±7 years) and in 15 healthy controls (53±2 years). All patients were on oral antidiabetic treatment (glyHb 6.3±0.9%) and not taking statins or anti-inflammatory drugs.
Results: In comparison with controls, the patients had a
higher waist circumference (1.08±0.09 <i>vs</i> 0.94±0.11 m, p<0.005) and higher fasting glucose (8.4±2.3 <i>vs</i> 5.3±0.7 mM, p<0.005), whereas fasting plasma lipids were not statistically different. The leukocyte count was higher in the patients (6.55±1.55 <i>vs</i> 5.07±1.10 x 10<sup>9</sup>cells/l, p<0.005) due to higher neutrophils and lymphocytes (+34% and +24%, p<0.05 for each). CD11B on monocytes and CD11B
and CD66B on neutrophils were higher in the patients
(+30%, +52% and +43%, p<0.05 for each). Fasting glucose, waist circumference, body mass index and systolic blood pressure were positively associated with the leukocyte and neutrophil count. The expressions of CD11B and CD66B on monocytes and neutrophils were strongly positively interrelated, but unrelated to TG and glucose.
Conclusion: In patients with type 2 diabetes, the expression of activation markers on monocytes and neutrophils is enhanced and not correlated to fasting glucose or TG. These results suggest a proinflammatory situation in type 2 diabetes and most likely represent increased adhesive capacity of neutrophils and monocytes to the endothelium.