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  • Title: Oral contraceptive steroids and atherosclerosis: lipogenesis in human arterial smooth muscle cells and dermal fibroblasts in presence of lipoprotein-deficient serum from oral contraceptive users.
    Author: Subbaiah PV, Bagdade JD.
    Journal: Artery; 1980; 6(6):437-57. PubMed ID: 7436743.
    Abstract:
    The incorporation of [14C]-acetate into lipids by cultured human arterial smooth muscle cells and dermal fibroblasts was studied in the presence of lipoprotein-deficient serum from oral contraceptive users (OC) and control women. Exposure to OC serum: 1) significantly increased the synthesis of cholesterol above controls in both fibroblasts (+25-56%) and smooth muscle cells (+28-42%) without a significant change in the synthesis of lecithin; and 2) resulted in increased cholesterol/lecithin ratios in newly synthesized lipids which were higher than controls in both fibroblasts (+50%) and smooth muscle cells (+30%). In vitro addition of the steroid ingredients of the "pill" to the growth medium containing control serum did not result in a stimulation of lipogenesis by the cells. [3H] - mevalonate incorporation into cholesterol was no different with OC and control serum, indicating that the stimulation noted in cholesterol synthesis by OC serum was due to an increased HMG-CoA reductase activity. These findings suggest that increased sterol synthesis in arterial smooth muscle cells of oral contraceptive users may be one pathogenetic factor which adversely influences their risk of atherosclerosis. Oral contraceptives users and control women sera were studied to determine the degree of incorporation of tritiated acetate into lipids by cultured human arterial smooth muscle cells and dermal fibroblasts. When the cells were exposed in vitro to oral contraceptive users serum, they showed a significant increase in synthesis of cholesterol above controls in both fibroblasts (increase of 25-26%) and smooth muscle cells (plus 28-42%) but no significant concomitant change in lecithin synthesis; this exposure also resulted in increased cholesterol/lecithin ratios in newly synthesized lipids much higher than controls in both fibroblasts (plus 50%) and smooth muscles (plus 30%). However, when steroid ingredients of the oral contraceptives were added in vitro to the growth medium containing control sera, no stimulation of lipogenesis by cells occurred. Tritiated mevalonate incorporation into cholesterol was no different with oral contraceptive user or control serum, indicating that the stimulation noted in cholesterol synthesis by oral contraceptive users serum was caused by an increased 3-hydroxy-3-methyl glutaryl-CoA reductase activity. This study suggests that increased sterol synthesis in arterial smooth muscle cells of oral contraceptive users may be a pathogenetic factor that affects the risk of atherosclerosis.
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