Biomedical subjects
Publications and source records attributed to G Silfverstolpe.
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11 oophorectomized women (mean age 34.5 +/- 5.9) were given the 17-C-alkylated ethinyl estradiol (EE) 20 microgram/day and the non-alkylated estrogen, estradioil valerianate (E2V) 2 mg/day for 6 weeks in separate periods preceded by 6 weeks without hormonal replacement therapy. Blood samples were drawn before and after 6 weeks on each estrogen. Serum phospholipids, cholesterol and triglycerides were assessed. Preparative ultracentrifugation with the isolation of the very low density (VLDL; d < 1.006 g/ml); the low density (LDL; d = 1.006-1.063 g/ml) and the high density lipoprotein (HDL; d > 1.063 g/ml) fraction was carried out. In the three lipoprotein fractions, phospholipid, total cholesterol, free cholesterol and triglycerides were determined. An oral glucose tolerance test with concomitant plasma insulin determination was performed. In the present study EE caused an increase in serum total and LDL triglycerides while there was a reduction of triglycerides in serum as well as in VLDL and LDL when E2V ws administered. There was a positive correlation between plasma insulin values during oral glucose tolerance test and serum and VLDL triglycerides when E2V was administered. This finding supports earlier studies indicating that insulin (or rather the insulin-glucagon relationship) influences the hepatic triglyceride production rate. Both EE and E2V increased HDL cholesterol, but E2V did not induce a concomitant increase in serum triglycerides which would suggest a more physiological effect from the latter compound since fertile females have lower serum triglycerides and higher HDL cholesterol levels than males of corresponding age. The same differences are true in a comparison between fertile and post-menopausal women.
Ten oophorectomized women (ranging in age from 27 to 45 years, having a mean age of 34.5 years with a standard deviation of 5.3) were given three different progestogens (norgestrel, norethisterone and medroxyprogesterone) in treatment periods of 3 weeks' duration immediately preceded by 3 weeks "wash out" periods. Venous blood samples were drawn before and after each treatment period. Free and total cholesterol, triglycerides and phospholipids were determined in the three lipoprotein fractions: Very low density lipoproteins (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL). Individual phosphatides were determined after thin layer chromatography. In addition, the relative fatty acid composition of serum lecithin and cholesterol esters were assessed by gas-liquid-chromatography. Both norethisterone and norgestrel caused a decrease in alpha-lipoprotein cholesterol. The relative fatty acid composition of serum lecithin revealed an increase of biochemical pathway 1 for liver lecithin synthesis on norgestrel and norethisterone but no major changes on medroxyprogesterone. With norgestrel an increase in serum-lysolecithin concomitant with a decrease in lecithin was observed, while the two other progestogens did not induce any significant changes. From the present data it is suggested that the 19-norethisterone derivatives, norethisterone and especially norgestrel, have androgen-like influences on lipid metabolism. Medroxyprogesterone, being a 17-alpha-hydroxyprogesterone, caused less changes and consequently less disturbance of lipid metabolism.