Α. Mikellidi, T. Nomikos
Platelets, apart from being cellular mediators of thrombosis that occurs at the late stages of atherosclerosis, they are actively involved in the early phases of the disease. A chronic, subclinical activation of platelets may play a crucial role in the development of the atherosclerotic plaque. Postprandial dysmetabolism could play the role of the daily platelet stimulant since it induces a pro-inflammatory and pro-oxidative environment in the endothelium which favors platelet activation. The effects of alimentary or oral glucose load hyperglycemia/hyperinsulinemia on platelet functions are contradictory and depend on the functional marker that is determined and the clinical profile of the volunteers. In general, the homeostatic mechanisms of healthy people prevent the postprandial activation of platelets while the platelets of metabolic syndrome or diabetic patients are more susceptible to acute hyperglycemic increments compared to healthy ones. A similar pattern is observed for postprandial hyperlipidemia. Oxidative stress, impairment of insulin’s antiplatelet actions, activation of platelet by triglyceride-rich lipoproteins remnants, reduced bioavailability of NO and alterations of the calcium and magnesium homeostasis are some of the mechanism that explain the postprandial modulation of platelets. Nutritional and pharmacological interventions, aiming to attenuate postprandial platelet responses, may have a beneficial role on atherosclerosis development.
Keywords: atherosclerosis, hyperglycemia, hyperlipidemia,oxidative stress, platelets, postprandial state