Thoracic Aorta

Chronic hyperinsulinemia is suspected of enhancing the development of arterial diseases. However, direct metabolic effects of insulin on the inner arterial wall are poorly documented. To assess the possible influence of variations in smooth muscle phenotype, we measured lipogenesis from glucose by rat thoracic aortas that had been injured with a balloon catheter. Aortas were exposed to insulin during either a 1-hour incubation or a 9-minute perfusion. Injury transiently stimulated lipogenesis by the intima-media (by 111% and 225% on the second day after injury in two separate experiments). However, insulin added either to the incubation medium or to the perfusion medium, even at a very high concentration (10 /iunits/ml), did not modify lipogenesis by the intima-media as long as 14 days after injury. In contrast, two days after injury, the adventitia responded to insulin in a dose-dependent manner. We conclude that: 1) Injury transiently stimulates lipogenesis from glucose by the intimamedia. 2) The change in smooth muscle cell phenotype, from contractile to synthetic, does not influence the metabolic sensitivity of the intima-media to insulin. 3) Our results do not substantiate the view that insulin contributes to the development of cardiovascular diseases through a direct lipogenic effect on arterial smooth muscle cells. (Arteriosclerosis and Thrombosis 1991;ll:91-96)