TY - JOUR
T1 - Sex and depot-specific stimulation of creatine kinase B in rat adipose tissues by gonadal steroids
AU - Sömjen, D.
AU - Lundgren, S.
AU - Kaye, A. M.
N1 - Funding Information:
Acknowledgements--tWhaen k Dr Nava Nevo for performingt he ovarectomieMs,s Liat Ben Yehoshuaf or the progesterondea ta, and Ms Rona Levin and Celina Gross for processingth e manuscript.T his work was supportedin partb y a grantf rom the Israel Cancer Association.D r S. Lundgren was the recipiento f a NorwegianC ancerS ocietyF ellowshipA. MK is the JosephM oss Professoor f MolecularE ndocrinology.
PY - 1997/5
Y1 - 1997/5
N2 - We report a sex- and depot-specific response of rat adipose tissues to gonadal steroids. The epididy-mal fat pad in male rats responded to androgens (testosterone and dihydrotestosterone; DHT), but not to 17β-estradiol (E2), by increased specific activity of the brain type isozyme of creatine kinase (CK). In female rats, the parametrial fat as well as the fat surrounding the spleen responded to E2 but not to dihydrotestosterone. In both sexes, subcutaneous fat from the inguinal, abdominal or thigh region did not respond to any sex steroid. The parametrial fat showed increasing responsiveness to E2 during postnatal development, in parallel to the response of the uterus. In cycling female rats, parametrial fat showed the highest basal activity of CK at estrus; stimulation by E2 was achieved on all,the other days of the cycle. Both phytoestrogens and diethylstilbestrol stimulated CK activity in both parametrial and spleen fat, in parellel to their estrogenic potencies, parametrial fat also responded to progesterone. The stimulation of CK activity in parametrial fat by E2 was completely blocked by actinomycin D or cycloheximide. Treatment with the antiestrogen, tamoxifen, caused moderate stimulation of CK activity in parametrial fat as well as partial inhibition of E2 stimulation of CK activity; the 'pure' antiestrogen ICI 164,384 had no agonistic effect and completely blocked the E2 effect. Ovariectomy caused an increased response to E2 without changes in the basal CK activity, but did not lead to any response to DHT. As well as being a reliable response marker, the differential modulation of CK activity can thus serve to distinguish adipose cells from different sources.
AB - We report a sex- and depot-specific response of rat adipose tissues to gonadal steroids. The epididy-mal fat pad in male rats responded to androgens (testosterone and dihydrotestosterone; DHT), but not to 17β-estradiol (E2), by increased specific activity of the brain type isozyme of creatine kinase (CK). In female rats, the parametrial fat as well as the fat surrounding the spleen responded to E2 but not to dihydrotestosterone. In both sexes, subcutaneous fat from the inguinal, abdominal or thigh region did not respond to any sex steroid. The parametrial fat showed increasing responsiveness to E2 during postnatal development, in parallel to the response of the uterus. In cycling female rats, parametrial fat showed the highest basal activity of CK at estrus; stimulation by E2 was achieved on all,the other days of the cycle. Both phytoestrogens and diethylstilbestrol stimulated CK activity in both parametrial and spleen fat, in parellel to their estrogenic potencies, parametrial fat also responded to progesterone. The stimulation of CK activity in parametrial fat by E2 was completely blocked by actinomycin D or cycloheximide. Treatment with the antiestrogen, tamoxifen, caused moderate stimulation of CK activity in parametrial fat as well as partial inhibition of E2 stimulation of CK activity; the 'pure' antiestrogen ICI 164,384 had no agonistic effect and completely blocked the E2 effect. Ovariectomy caused an increased response to E2 without changes in the basal CK activity, but did not lead to any response to DHT. As well as being a reliable response marker, the differential modulation of CK activity can thus serve to distinguish adipose cells from different sources.
UR - http://www.scopus.com/inward/record.url?scp=0343471972&partnerID=8YFLogxK
U2 - 10.1016/S0960-0760(97)00011-3
DO - 10.1016/S0960-0760(97)00011-3
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AN - SCOPUS:0343471972
SN - 0960-0760
VL - 62
SP - 89
EP - 96
JO - Journal of Steroid Biochemistry and Molecular Biology
JF - Journal of Steroid Biochemistry and Molecular Biology
IS - 1
ER -