Kazama Y, Noguchi T, Kanemaru Y, Wakasugi M, Onaya T, Yoshida Y
Third Department of Internal Medicine, University of Yamanashi Medical School, Japan.
Prostaglandins Leukot Essent Fatty Acids. 1989 Aug;37(2):129-34. doi: 10.1016/0952-3278(89)90109-9.
We have investigated the effects of insulin on the synthesis of prostacyclin and cell proliferation in cultured vascular smooth muscle cells, which have been thought to play important roles in the development of atherosclerosis. Prostacyclin was measured as 6-keto-PGF1 alpha in the culture medium, and cell proliferation as incorporation of [3H]thymidine into DNA. Our studies showed that insulin reduced production of prostacyclin and stimulated cell proliferation in SMC. Like insulin, dibutyryl cAMP inhibited the production of prostacyclin, whereas it did not stimulate cell proliferation. No significant changes in cAMP levels were found on the addition of insulin into the culture medium. Therefore, cAMP does not appear to be involved in the mechanisms of these insulin effects. These results again suggest that hyperinsulinemia could be one of the important factors in atherosclerosis.
