PubMed Health⌕ Search

Biomedical subjects

Veera Vihma

Publications and source records attributed to Veera Vihma.

4 recordsLinked to original sources

Postmenopausal estrogen therapy and serum estradiol fatty acid esters in women with and without previous intrahepatic cholestasis of pregnancy.

BACKGROUND: Fatty acid esters of 17beta-estradiol (E2) are estrogen metabolites associated with lipoproteins in blood. AIM: To study the effects of estrogen therapy on concentrations of serum E2 fatty acid esters in postmenopausal women with a history of an estrogen-related liver disorder, intrahepatic cholestasis of pregnancy (ICP), and in healthy women in a double-blind, crossover fashion. METHOD: ICP (n = 10) and control women (n = 10) received increasing doses of E2 valerate orally 2-4 mg/day, or transdermal E2 50-100 microg/day for 6 weeks. After a 4-week wash-out period, the subjects crossed over to the alternate E2 treatment. Concentrations of serum E2 fatty acid esters were quantified after saponification by fluoroimmunoassay. RESULTS: Oral E2 administration increased median serum E2 fatty acid ester concentrations from 57 to 73 pmol/L in the ICP and from 56 to 74 pmol/L in the control group, in association with elevations in serum E2, estrone and sex hormone-binding globulin levels. Transdermal E2 treatment did not increase serum E2 ester levels. CONCLUSIONS: The increase in serum E2 fatty acid esters during oral E2 administration may be attributed, at least partly, to the higher estrogen dose during oral compared with transdermal therapy. A history of ICP did not affect esterification of E2 during estrogen therapy.

Case-Control Studies↗

Differential effects of oral and transdermal estradiol treatment on circulating estradiol fatty acid ester concentrations in postmenopausal women.

Estradiol fatty acid esters are potent lipophilic estrogens with antioxidant properties, transported by lipoproteins in blood. We investigated effects of oral and transdermal estradiol replacement therapy on concentrations of estradiol fatty acid esters in serum in postmenopausal women in a double-blind, randomized fashion. The first group (n = 9) received oral (2 mg/d); the second (n = 10), transdermal estradiol (patch delivering 50 microg/d); and the third group (n = 7), placebo treatment for 12 wk. After extraction of serum and separation of esterified estradiol from nonesterified estradiol, the concentration of saponified estradiol esters was measured by time-resolved fluoroimmunoassay. In the oral estradiol group, the median serum estradiol fatty acid ester concentration rose by 27%, from 77 to 98 pM (P = 0.028) but remained unchanged in the transdermal estradiol and placebo groups. The median concentrations of serum nonprotein-bound estradiol increased similarly in the oral and transdermal estradiol groups. The change in serum estradiol ester concentrations during treatment, but not that of nonesterified estradiol, correlated positively with enhanced forearm blood flow responses in vivo. These data raise the possibility that an increase in serum estradiol fatty acid esters may contribute to beneficial effects of oral estradiol treatment, compared with an equipotent dose of transdermal estradiol.

Administration, Cutaneous↗

Quantitative determination of estradiol fatty acid esters in lipoprotein fractions in human blood.

According to experimental studies, 17 beta-estradiol associates with lipoproteins in blood in the form of fatty acid esters. However, concentrations of endogenous estradiol esters in human lipoprotein fractions have not been previously reported. We investigated the distribution of estradiol fatty acid esters between plasma lipoproteins in 10 healthy women during late pregnancy. Following extraction from serum and ultracentrifugally isolated, gel-filtered lipoproteins, estradiol esters were separated from nonesterified estradiol by column chromatography. After saponification and chromatographic purification of the estradiol ester fraction, the concentration of hydrolyzed esters was determined by estradiol time-resolved fluoroimmunoassay. Of total serum estradiol, a mean of 0.7% (549 pmol/liter, n = 10) was in the form of fatty acid esters. Estradiol fatty acid ester concentrations measured in serum and lipoprotein fraction correlated positively (n = 10; r = 0.98; P < 0.001). The majority of lipoprotein estradiol esters, 54%, was recovered in high-density lipoprotein, and 28% in low-density lipoprotein fraction. Most lipoprotein fractions contained undetectable amounts of nonesterified estradiol (< 36 pmol/liter). In conclusion, our results indicate that estradiol fatty acid esters are mostly bound by lipoproteins in blood in vivo.

Adult↗

Lipoprotein-associated estrogens.

The discovery of a family of hormonal steroids esterified with fatty acid has raised questions concerning their physiologic role. Because of their water-insolubility these compounds are present in the circulation only as components of lipoprotein particles. Current evidence supports the hypothesis that estrogen esterification is catalyzed by lecithin:cholesterol acyltransfearse associated with HDL. In addition, recent results indicate that estradiol esters are transferred from HDL to LDL particles in a cholesteryl ester transfer protein (CETP)-associated process. The studies now focus on the various possible physiologic roles proposed for these hormone derivatives, (1) functioning as fat-soluble antioxidants incorporated in lipoproteins rendering protection against oxidation of these particles, (2) providing a mechanism for hormonal storage in lipoproteins and fat tissues, (3) providing a novel hormone transport system using lipoprotein as carriers and lipoprotein receptors for entry into cells. Quantitative methods of determination of estradiol fatty acid esters in human body fluids have been developed. Preliminary studies suggest that diet-derived plant estrogens may also form fat-soluble derivatives which become incorporated in lipoproteins.

Antioxidants↗