The oxidation of low density lipoproteins (LDLs) is thought to take place in the arterial intima when the particles have become isolated from circulating water-soluble antioxidants. We hypothesized that isof lavonoid antioxidants derived from soy could be incorporated into lipoproteins and possibly could protect them against oxidation, which is regarded as atherogenic. Six healthy volunteers received 3 soy bars [containing the isof lavonoid antioxidants genistein (12 mg) and daidzein (7 mg)] daily for 2 weeks. LDLs were isolated from blood drawn at the the end of a 2-week dietary baseline period, after 2 weeks on soy, and after discontinuation of soy. Large increases in plasma isof lavonoid levels occurred during soy feeding, but only minute amounts were stably associated with lipoproteins (less than 1% of plasma isof lavonoids in the LDL fraction). The LDLs were subjected to copper-mediated oxidation in vitro. Compared with off soy values, lag phases of LDL oxidation curves were prolonged by a mean of 20 min (P < 0.02) during soy intake, indicating a reduced susceptibility to oxidation. The results suggest that intake of soyderived antioxidants, such as genistein and daidzein, may provide protection against oxidative modification of LDL. As only very small amounts of these substances were detected in purified LDL, modified LDL particles may have been produced in vivo by circulating isof lavonoids promoting resistance to oxidation ex vivo.
Both estrone and estradiol production in visceral AT increased with adiposity, but estradiol was produced more effectively in subcutaneous fat. Both AT depots produced estrone from E1S. Increasing visceral adiposity could increase overall estrogen exposure in postmenopausal women.
Estrogen metabolism is differentially regulated in the adipose tissue of women with or without cancer. In the sc adipose tissue proximal to breast tumor 17β-hydroxysteroid dehydrogenase type 12 expression is lower than in controls, which could indicate that the conversion of estrone to estradiol is decreased. Further studies are needed to establish the clinical significance of our findings in the development and growth of breast cancer in postmenopausal women.
The production of E₂ by the large adipose mass was not reflected by increased circulating E₂ concentrations in severely obese men or women. However, adipose tissue may contribute to concentrations of serum E₂-FAE.
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.
The overall higher ester to free estradiol ratio in adipose tissue than in serum indicates active esterification capacity in adipose tissue. The predominance of esterified and free estradiol in postmenopausal adipose tissue compared with serum suggests in situ production and storage. Whether the estradiol esters have an independent physiological role in adipose tissue remains to be clarified.
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