The Journal of reproductive medicine · 2002
The FORKO mouse as a genetic model for exploring estrogen replacement therapy.
Оценочное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Sairam M Ram, Danilovich Natalia, Lussier-Cacan Suzanne
Аннотация
OBJECTIVE: To evaluate how chronically estrogen deficient female FORKO mice with genetic disruption of the FSH receptor respond to estrogen therapy.
STUDY DESIGN: Subcutaneous estrogen agonist or antagonist therapy was initiated to study reproductive tissue response, adipose tissue mass and plasma lipid profiles.
RESULTS: Within 36-48 hours of agonist administration, the classic measures of estrogenic activity were evident in the uterus and vagina. Older animals also responded to therapy during a 10-day period, indicating that estrogen receptor signaling systems are unaffected by aging. In these obese mutants, this short treatment decreased adipose tissue in all areas and corrected lipid abnormalities. Tamoxifen, a nonsteroidal mixed estrogen agonist and antagonist, had marginal effects on the uterus and body fat of FORKO mice, indicating differences in interaction.
CONCLUSION: In FORKO mice lacking ovarian estrogen, the receptors remain fully functional. Hence, this is a useful model for studying estrogen replacement therapy and helps resolve questions related to efficacy and actions.
STUDY DESIGN: Subcutaneous estrogen agonist or antagonist therapy was initiated to study reproductive tissue response, adipose tissue mass and plasma lipid profiles.
RESULTS: Within 36-48 hours of agonist administration, the classic measures of estrogenic activity were evident in the uterus and vagina. Older animals also responded to therapy during a 10-day period, indicating that estrogen receptor signaling systems are unaffected by aging. In these obese mutants, this short treatment decreased adipose tissue in all areas and corrected lipid abnormalities. Tamoxifen, a nonsteroidal mixed estrogen agonist and antagonist, had marginal effects on the uterus and body fat of FORKO mice, indicating differences in interaction.
CONCLUSION: In FORKO mice lacking ovarian estrogen, the receptors remain fully functional. Hence, this is a useful model for studying estrogen replacement therapy and helps resolve questions related to efficacy and actions.