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Diabetes is an elevated PGE2 condition: clues for protective therapies Diabetes is a major health issue in the developed and developing world and is linked with vascular complications and a high incidence of cardiovascular disease such as myocardial infarction. In the current study we examined plasma PGE2 levels in type 1 and type 2 diabetic patients as PGE2 is implicated in atherosclerotic plaque destabilization via metalloproteinase activation. Further PGE2 inhibits lipolysis in white adipose tissue and may have a central role in obesity and the metabolic syndrome. Plasma prostaglandins were measured using enzyme linked immunoassays and monocyte COX-2 by western blotting. In type 1 diabetic patients (n=19) PGE2 levels were elevated 2.7 fold compared to non diabetic controls and in aged matched type 2 diabetic patients (n=19) the PGE2 levels were elevated 2.6 fold relative to age matched non diabetic controls. In type 1 diabetic patients the COX-2 expression in monocytes was elevated by 35% but in type 2 diabetic patients monocyte COX-2 was not altered. Thus the source of the PGE2 may not be the same in both conditions. Plasma thromboxane B2 was not altered in either diabetic group. Diabetes appears to be an elevated PGE2 condition. Diabetic patients on aspirin therapy had lower levels of PGE2 and this may contribute to aspirin’s protective role. However, it may be that drugs targeting PGE2 through the various EP receptors may more selectively reduce cardiovascular risk. EP4 receptors are involved in matrix metalloproteinase release that promotes plaque instability (1) and EP3 receptors in obesity related effects (2).
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