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Department of Animal Science, University of California, Davis 95616
ABSTRACT
A genetic deficiency associated with a low growth rate, high neonatal mortality, and lowered fertility has been studied in an inbred strain of Jersey cattle. The delayed puberty, lowered fertility, slow growth rate, and the response to supplementary Cortisol indicate that the syntheses and secretion of Cortisol and the sex steroids are deficient. Homogenates from the adrenal cortex incubated with progesterone 4-14C revealed that the deficient animals converted progesterone to 17
-hydroxyprogesterone, 11-deoxycortisol, and Cortisol less efficiently than homogenates from normal animals of the same strain and from unrelated Holsteins. It is concluded that the primary metabolic deficiency in these animals is the subnormal production of 17
-hydroxyprogesterone and that the low production of the other steroids results from this primary deficiency.
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