Nonesterified Fatty Acids, Albumin, and Platelet Aggregation

Independent and Combined Effects of Serum Albumin and C-Reactive Protein on Long-Term Outcomes of Patients Undergoing Percutaneous Coronary Intervention

“…33 Serum albumin has also been reported to be a specific inhibitor of human endothelial apoptosis 34 and a significant inhibitor of platelet activation and aggregation. 35 Malnutrition is a complex state involving reduction of protein reserves, caloric collapse, and weakening of immune defenses. The MIA syndrome describes the high correlation of 3 significant separate clinical entities, namely malnutrition, inflammation, and atherosclerosis, which coexist in patients with CKD, especially ESRD.…”

Free Fatty Acid Is Associated with Thrombogenicity in Cardioembolic Stroke

“…Free fatty acids (FFAs), in addition to their role as energy fuel and an important metabolite of lipid metabolism [1], have other important biological activities, such as the regulation of platelet activation and thrombosis [2]. The causal relationship of elevated FFA levels with thrombogenesis was proved in the earlier animal studies [3,4], and the factors responsible for the thrombogenic effect of FFAs appear to be multiple, and include oxidative stress, increased inflammation, decreased nitric oxide with reduced vasodilatation, and platelet activation associated with the arachidonic acid pathway [2].…”

“…The causal relationship of elevated FFA levels with thrombogenesis was proved in the earlier animal studies [3,4], and the factors responsible for the thrombogenic effect of FFAs appear to be multiple, and include oxidative stress, increased inflammation, decreased nitric oxide with reduced vasodilatation, and platelet activation associated with the arachidonic acid pathway [2]. …”

Dynamic modulation of platelet aggregation, albumin and nonesterified fatty acids during physical exercise in Thoroughbred horses

“…The increase of NEFAs values found after exercise represents a metabolic response of the horse to physical exercise and may be due to the known low ability of Thoroughbred horses to use lipids as energy substrate (Pösö et al 1989;Assenza et al 2012). It was suggested that any condition that leads to an increase in NEFAs levels could contribute to platelet hyperactivity (Dhindsa et al 2015). Effectively, higher NEFAs concentration could lead to a reduction of stability of prostacyclin generated by endothelium (Dhindsa et al 2015), which is a strong inhibitor of platelet aggregation.…”

“…Despite the well-characterized factors modulating platelet activity, several studies carried out on experimental animal models and in humans have shown that albumin and nonesterified fatty acids (NEFAs) have an opposite role in the activation of platelets and thrombosis (Dhindsa et al 2015). Particularly, high levels of NEFAs lead to massive thrombosis and platelet activation (Connor et al 1963;Burstein et al 1978), whereas their binding to albumin protects the platelets from activation (Nordoy 1979).…”