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Departments of Biochemistry and Experimental Medicine, McGill University, and University Clinic, Royal Victoria Hospital Montreal, Quebec H3A 1A1, Canada
Address requests for reprints to: Dr. Samuel Solomon, Endocrine Laboratory, Room L205, Royal Victoria Hospital, Pine Avenue West, Montreal, Quebec H3A 1A1, Canada.
Abstract
The metabolism of [3H]progesterone by the fetal calf adrenal was examined in homogenates and microsomal fractions of adrenals obtained from mid- or late gestational fetal calves. Throughout the course of gestation, there was no detectable difference in the formation of corticosterone from progesterone by adrenal homogenates. In contrast, cortisol production in these same homogenates increased 7-fold from 0.3–2.2% at the end of gestation. Similar results were obtained using microsomal fractions prepared from these homogenates: the 17
-hydroxylation of progesterone (i.e. 17
-hydroxyprogesterone and 11-deoxycortisol) increased from 0.7% to 26% at the end of gestation.
The results suggest that the increased cortisol observed in the fetal circulation toward the end of gestation is the result of a rapid increase in the capacity of the fetal calf adrenal to form 17
-hydroxycorticosteroids. The underlying mechanism for this change is discussed. (Endocrinology 113: 1077,1983)
Footnotes
* This work was supported by the MRC of Canada, Grant MT1658, USPH Grant HD04365, and the National Foundation March of Dimes Grant 1–694.
Current address: Orthopedic Research Laboratory, Royal Victoria Hospital, Montreal, Quebec HA3 1A1, Canada.
Current address: Laboratories for Neuroendocrinology, Salk Institute for Biological Studies, La Jolla 92138, California.
Received August 27, 1982.
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