Sitagliptin Therapy and Kinetics of Inflammatory Markers
Status:
Completed
Trial end date:
2017-10-31
Target enrollment:
Participant gender:
Summary
Inflammatory processes are increasingly being recognized as a critical step in the
pathogenesis of both diabetes and heart disease and may constitute a biological link between
the two diseases. Inflammatory cytokines increase vascular permeability, change
vasoregulatory responses, increase leukocyte adhesion to endothelium, and facilitate thrombus
formation by inducing procoagulant activity, inhibiting anticoagulant pathways, and impairing
fibrinolysis. Leukocyte adhesion to arterial endothelial cells is thought to be an important
step in the development of atherosclerosis, and adhesion molecules, such as intercellular
adhesion molecule-1 (ICAM-1) and L-selectin, play key roles in this process. Therefore,
identifying novel therapeutic approaches that would favorably affect inflammation,
endothelial function, and glucose is of significant interest. Investigators have recently
demonstrated that, relative to placebo, sitagliptin treatment resulted in a significant
reduction in plasma levels of various inflammatory markers and cell adhesion molecules. The
results also suggest that the beneficial effects of sitagliptin on both inflammation and
endothelial function are most likely mediated by an elevation in plasma GLP-1 levels and
global improvement of the glucose-insulin homeostasis. However, the mechanisms underlying the
beneficial effects of sitagliptin on these markers remain to be fully elucidated. The
proposed study will address this key issue.