Rat female derived adipose tissues respond to estrogens and vitamin D metabolites of in vivo
Dalia Somjen1,2 & Alvin M Kaye1,2
We have previously reported that treatment in vivo with estrogenic compounds or vitamin D metabolites increased the specific activity of creatine kinase specific activity (CK) in different organs both in intact and in ovariectomized female rats. In the present study we assessed the hormonal responsiveness of para-uterine fat from female and epididymal fat from male rats. Injection of immature female rats with 5 μg estradiol-17β (E2), 50 μg of estrone (E1), 50 μg estriol (E3), 500 μg diethylstilbestrol (DES), 500 μg cumestrol (Cum) or 50 μg genistein (G) resulted in increased CK by all compounds tested- When female rats were injected with different anti-estrogens only tamoxifen stimulated CK in fat, whereas raloxifene, tamoxifen methiodide or ICI 164 384 were ineffective, but inhibited E2- stimulated CK. Injection of female rats with E2 at different days of the menstrual cycle resulted in highest increased CK in proestrous, lower response in diestrous, even lower at metestrous and no response at oestrous. E2 induced CK in the para-uterine fat of immature rats was age dependent and was active after ovariectomy with increased response at different time after surgery. CK induction by E2 was inhibited by both inhibitors of protein and RNA synthesis. Induction of diabetes lead to increased CK in para-uterine fat, but to abolishmed response to E2. Fat cells from either intact female or male as well as gonadectomised rats responded to injection of either 0.5 ng of 1, 25(OH)2D3 or 5 ng 24, 25(OH)2D3 with increased CK. In conclusion, fat tissues from female rats both intact and after ovariectomy, responded to different estrogens and vitamin D metabolites by increased CK similar to the uterus itself. Since fat cells express ERs mRNA, it might be considered as a new target for estrogens and has to be considered when treated with HRT, both for its beneficial and hazardous effects.