Treatment with estrogenic compounds or vitamin D metabolites and analogs increased the specific activity of creatine kinase (CK) in different organs from intact or ovariectomized female rats. We now assessed the hormonal responsiveness of para-uterine fat from female rats. Injection or feeding of immature female rats with different estrogens resulted in increased CK. Injection with anti-estrogens resulted in tamoxifen stimulated CK, whereas all others were effective only in inhibition of E2-stimulated CK. E2 injection at different days of the menstrual cycle resulted in highest increased CK in pro-estrous, lower response in di-estrous and met-estrous and no response at estrous. E2 induced-CK was age-dependent and increased at different time after ovariectomy. CK induction by E2 was abolished by inhibitors of both protein and RNA synthesis. Induction of diabetes led to decreased basal CK in para-uterine fat, with no hormonal response. Fat cells responded to the vitamin D metabolites 1,25(OH)2D3 (0.5 ng) or 24,25(OH)2D3 (5 ng) and to the non-hypercalcemic analogs of 1,25(OH)2D3 i.e. hexa-fluoro vitamin D3 (FL), the side chain modified derivatives: EB 1089 (EB), CB 1093 (CB) and MC 1288 (MC), or the less-calcemic analogs: JK1624F2-2 (JKF) and QW1624F2-2 (QW). But these analogs unlike other organs and similar to the uterus, did not up-regulate the response to E2. In conclusion, rat female derived fat tissues responded to estrogenic compounds and to vitamin D metabolites and analogs, by increased CK and should be considered as a target for both the beneficial and the hazardous effects of hormonal treatments.
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