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Dietary sources of lignans and isoflavones modulate responses to estradiol in estrogen reporter mice
Author(s) -
PenttinenDamdimopoulou Pauliina E.,
Power Krista A.,
Hurmerinta Teija T.,
Nurmi Tarja,
van der Saag Paul T.,
Mäkelä Sari I.
Publication year - 2009
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200800487
Subject(s) - phytoestrogens , enterolactone , isoflavones , genistein , estrogen , endocrinology , medicine , lignan , biochanin a , estrogen receptor , ovariectomized rat , transactivation , biology , daidzein , chemistry , biochemistry , gene expression , cancer , breast cancer , botany , gene
Dietary phytoestrogens, such as the lignan metabolite enterolactone (ENL) and the isoflavone genistein (GEN), are suggested to modulate the risk of estrogen‐dependent disease ( e.g ., breast cancer) through regulation of estrogen signaling. However, the effects of complex food items containing lignans or isoflavones on estrogen receptor (ER) transactivation have not been assessed so far. In this study, the modulation of ER‐mediated signaling by dietary sources of lignans (cereals and flaxseed) and isoflavones (soy) was studied in vivo . Adult ovariectomized 3×ERE‐luciferase (luc) reporter mice received isocaloric diets supplemented with flaxseed, rye, wheat, or soy for 40 h or two weeks, and an additional group of mice was challenged with 17β‐estradiol (E 2 ) following the two‐week dietary intervention. In non‐E 2 ‐treated mice, soy diet induced luc expression in liver, mammary gland, and pituitary gland while the other diets had no effects. Interestingly, all diets modulated the E 2 ‐induced luc expression. In particular rye diet efficiently reduced E 2 ‐induced luc expression as well as uterine growth, the hallmark of estrogen action in vivo . It is concluded that dietary sources of lignans and isoflavones can modulate estrogen signaling in vivo . The results suggest intriguing possibilities for the modulation of the risk of estrogen‐dependent diseases by dietary means.