Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Relationship of Endogenous Sex Steroid Hormones to Lipids and Apoproteins in Postmenopausal Women

Relationship of Endogenous Sex Steroid Hormones to Lipids and Apoproteins in Postmenopausal Women The relationships between blood levels of estrogen and lipoprotein lipids and apoproteins were evaluated in 120 women early in the climacteric. Among women who were 1-year amenorrheic, not taking hormone replacement therapy, and with follicle-stimulating hormone levels >720 ng/ml, serum estradioi levels were positively related to concentrations of the high density lipoprotein 2 cholesterol (HDL2c) subfraction. There was a substantial decrease in HDL2c and apoprotein (apo) A-l in women whose estradioi levels decreased to <2.5 pg/ml from the first to the second postmenopausal examination. In a sample of women evaluated during the perimenopause (3-months&apos; amenorrheic), those with the highest concentrations of estradioi or estrone showed a (nonsignificantly) higher level of HDL2c and a lower level of low density lipoprotein cholesterol (LDLc) than did those with the lowest concentration of estradioi or estrone. Estradioi levels declined dramatically between the perimenopausal and the postmenopausal examinations, and this was accompanied by a decrease in HDL2c and a nonsignificant increase in LDLc. HDL2c levels fell substantially in those women whose estradioi decreased below the sensitivity of the assay. The change, however, was not statistically significant. Estrone is the primary postmenopausal estrogen, and levels are directly related to obesity, as are levels of insulin. The interrelationship among obesity, conversion of estrone to estradioi at the tissue level, and insulin (or insulin sensitivity) is probably the primary determinant of HDLc concentration among postmenopausal women. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis Wolters Kluwer Health

Relationship of Endogenous Sex Steroid Hormones to Lipids and Apoproteins in Postmenopausal Women

Loading next page...
 
/lp/wolters-kluwer-health/relationship-of-endogenous-sex-steroid-hormones-to-lipids-and-aKWM1F1y0l

References

References for this paper are not available at this time. We will be adding them shortly, thank you for your patience.

Copyright
© 1990 by American Heart Association, Inc.
ISSN
0276-5047

Abstract

The relationships between blood levels of estrogen and lipoprotein lipids and apoproteins were evaluated in 120 women early in the climacteric. Among women who were 1-year amenorrheic, not taking hormone replacement therapy, and with follicle-stimulating hormone levels >720 ng/ml, serum estradioi levels were positively related to concentrations of the high density lipoprotein 2 cholesterol (HDL2c) subfraction. There was a substantial decrease in HDL2c and apoprotein (apo) A-l in women whose estradioi levels decreased to <2.5 pg/ml from the first to the second postmenopausal examination. In a sample of women evaluated during the perimenopause (3-months&apos; amenorrheic), those with the highest concentrations of estradioi or estrone showed a (nonsignificantly) higher level of HDL2c and a lower level of low density lipoprotein cholesterol (LDLc) than did those with the lowest concentration of estradioi or estrone. Estradioi levels declined dramatically between the perimenopausal and the postmenopausal examinations, and this was accompanied by a decrease in HDL2c and a nonsignificant increase in LDLc. HDL2c levels fell substantially in those women whose estradioi decreased below the sensitivity of the assay. The change, however, was not statistically significant. Estrone is the primary postmenopausal estrogen, and levels are directly related to obesity, as are levels of insulin. The interrelationship among obesity, conversion of estrone to estradioi at the tissue level, and insulin (or insulin sensitivity) is probably the primary determinant of HDLc concentration among postmenopausal women.

Journal

ArteriosclerosisWolters Kluwer Health

Published: Nov 1, 1990

There are no references for this article.