Background: The leading causes of morbidity and mortality among patients with type 2 diabetes mellitus (T2DM) are cardiovascular atherosclerosis, peripheral arterial disease and cerebrovascular diseases. The accumulation of platelet plugs at sites of atherosclerotic lesion rupture is the most common mechanism leading to myocardial or cerebral infarction. Platelets from diabetic patients are activated. We previously demonstrated that high platelet aggregation is associated with high HbA1c levels and vitamin D deficiency. We also found that calcitriol (vitamin D-1,25) directly reduced platelet aggregation in T2DM. Omentin-1, also known as intelectin, is a new adipokine, strongly expressed in visceral adipose tissue. Serum omentin-1 levels are decreased in obese individuals and T2DM. Omentin-1 exerts anti-inflammatory and anti-atherogenic function in endothelial and smooth-muscle cells. Additionally, omentin-1 inhibits inflammation and attenuates monocyte adhesion in endothelial cells.
Aim: To study the effect of calcitriol and omentin-1 on ADP-induced, platelet P-selectin expression and platelet-leukocyte-aggregate formation at various glucose levels in vitro.
Methods: Blood samples were collected from healthy volunteers. Whole blood or platelet rich plasma (PRP) was pre-treated with 50mM glucose for 20 minutes in the presence of calcitriol or omentin-1. Platelets were activated by 5mM ADP. CD62p expression (P-selectin) and CD61+/CD14+ cells (platelet-monocyte-aggregate) were detected by flow cytometry.
Results: In vitro, glucose treatment enhanced platelet activation induced by ADP. These preliminary results indicate that omentin-1 reduces platelet-leukocyte aggregation with and without glucose. Calcitriol was also found to affect platelet activation, as it slightly reduced both p-selectin expression and platelet-monocyte-aggregation.
Conclusions: This study indicates a role for omentin-1 as a regulator of platelet- leukocyte interactions. These results support our previous findings, indicating a direct effect of calcitriol on platelet activation.