Estrogen inhibition of adrenocortical function in the lactating dairy cow
Creators: name: Mason, Steve
Publisher: name: University of British Columbia
Year: 2010

description: Acetonemia is a metabolic disorder common among dairy cattle in the period from 10 days to six weeks post partum. It is during this time that milk production is at its maximum and in addition, the cow is beginning to exhibit regular estrous cycles. Thus, the profound demands for the precursors of milk production are superimposed upon a relatively unstable endocrine environment. The initial objective of this study was a clarification of the interactions between estrogens and endogenous substrates of glucose metabolism in the lactating cow. Since estrogen levels during the bovine estrous cycle had not been convincingly reported at the outset of this work, their measurement was the subject of the first experiment. Both estradiol and estrone exhibited peaks on the two days prior to the day of standing heat. These findings were later substantiated with the appearance of reports where plasma estrogen levels were measured by competitive protein binding and radioimmunoassay. A significant decline in plasma amino nitrogen concentration occurred after the estrogen peak, the decrease being reflected in marked reductions in the concentrations of threonine, methionine, proline and the branched chain amino acids. A notable hypoglycemia occurred somewhat later than the decline in amino acids. These findings were rationalized in terms of increased uterine and mammary uptake and/or decreased tissue mobilization of amino acids which may have given rise to the hypoglycemia as a result of decreased availability of glucogenic substrate. A possible mechanism of decreased tissue mobilization of amino acids was considered to be the inhibition by estrogens of adrenal glucocorticoid output, since glucocorticoids play a major role in regulating amino acid balance in peripheral tissues. In addition, the efficacy of glucocorticoid therapy in the treatment of bovine acetonemia is well recognized. With these considerations in mind, the role of estrogens in the modification of ACTH-stimulated glucocorticoid secretion was assessed in two further experiments. Following suppression of endogenous ACTH secretion by dexametha-sone, both estrogen treated and non-estrogen treated cows were subjected to stimulation with incremental doses of exogenous ACTH. At all levels of ACTH stimulation, estrogen treatment resulted in reduced response when measured in terms of plasma glucocorticoid concentrations. However, estrogen treatment had no effect on plasma binding of glucocorticoids. The concentrations measured were, therefore, a direct reflection of glucocorticoid activity. In the second experiment to test adrenal inhibition by estrogens, plasma ACTH and glucocorticoid levels were measured during the estrous cycles of lactating cows. For this purpose, a radioimmunoassay for ACTH was developed, providing a sensitive, reproducible method for the measurement of this hormone in bovine plasma. A significant increase in circulating ACTH concentration was seen during the estrogenic phase of the estrous cycle. No such increase was noted in the concentration of glucocorticoids, levels fluctuating within the normal, low range. This result implied that during the estrogenic phase of the estrous cycle, inhibition of glucocorticoid secretion by estrogens resulted in a compensatory rise in circulating ACTH concentration, bringing the glucocorticoid level back to normal. The results of these experiments are discussed with reference to the possible role of alterations in endocrine balance in the etiology of bovine acetonemia.