We read with interest in a previous issue of Clinical Science the paper by Naderali et al.  concerning the nutritional induction of obesity in Wistar rats and the subsequent relationship between hypertriacylglycerolaemia and endothelial dysfunction. Acknowledging the difficulties of drawing inferences for humans from studies carried out in experimental animals, the paper raises several interesting issues concerning the mechanisms whereby an unfavourable diet may lead to obesity and vascular disease. We should like to offer the following observations and viewpoint. A principal correlate of endothelial dysfunction in the study appeared to be hypertriacylglycerolaemia. Hypertriacylglycerolaemia represents the accumulation of triacylglycerol-rich lipoproteins, some of which are atherogenic, e.g. chylomicron remnants, and others which are not, e.g. chylomicrons. The adverse effects of remnant lipoproteins on endothelial function and on clinical events have been shown previously in experimental  and human  studies respectively. Moreover, postprandial hypertriacylglycerolaemia may also be a consequence of the vascular insulin resistance of obesity , but whether this exclusively involves atherogenic lipoproteins remains unclear. Low high-density lipoprotein (HDL), a well-recognized reciprocal of hypertriacylglycerolaemia in obesity, has also been causally implicated in endothelial dysfunction . It is likely that low HDL would have exacerbated the potentially adverse effect of hyper-remnantaemia and other factors on the vasotonic responses noted in this study. One methodological drawback was that the authors did not specifically test in their ex vivo protocol the L-arginine}NO pathway by employing a specific inhibitor of NO synthase, such as NG-monomethyl-L-arginine. The possibility of a specific defect in this pathway is also questioned on the basis of the abnormal vasotonic response to sodium nitroprusside, an endotheliumindependent agonist. Vascular insulin resistance in vivo may also depend on an enhancement of endothelinmediated vasoconstriction .