Nonesterified fatty acids, albumin, and platelet aggregation.

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It has been known for five decades that nonesterified fatty acids (NEFAs) have a role in the activation of platelets and thrombosis. Thus, the infusion of NEFAs leads to massive thrombosis and platelet activation (1–4). It has also been shown that their binding to albumin protects the platelets from activation (5). Thus, it follows that a fall in the concentrations of albumin, as in the nephrotic syndrome, would potentially lead to platelet activation. This has been demonstrated in several studies (6). Similarly, any condition that leads to an increase in NEFAs or a decrease in plasma albumin concentrations or a combination of the two would contribute to platelet hyperactivity. Insulin is a potent antilipolytic hormone and thus insulin-resistant states are characterized by accelerated lipolysis and increased NEFA concentrations. This promotes platelet aggregation. In addition, elevated NEFA concentrations interfere with insulin signal transduction and induce insulin resistance (7). NEFAs also induce oxidative and inflammatory stress (8) and thus activate monocytes, which express the prothrombotic tissue factor (TF) on their cell membranes (9). TF activates the extrinsic pathway of thrombin generation and hence may precipitate thrombosis. Activated platelets in patients with diabetes and …