The effect of Dexa-methasone (DXM) on circulating testosterone and luteinizing hormone (LH) in young post-puberal bulls

Theriogenology (Impact Factor: 1.8). 03/1976; 5(2):53-60. DOI: 10.1016/0093-691X(76)90168-0
Source: PubMed


Testosterone (T) and luteinizing hormone (LH) in the peripheral plasma of 6 young postpubertal (52 weeks of age) bulls were measured by radioimmunoassay. For 3 bulls blood samples were collected at half-hour intervals for 6 hours one day before dexamethasone (DXM) injection (20 mg) and two days after. For the 3 others blood collection occurred two days before injection and two days after. On the days before treatment, T and LH concentrations fluctuated similarly to what was previously observed. After treatment LH decreased rapidly and remained between 0.25 and 1.0 ng/ml until the end of the experiment. We observed a small peak of T (between 1.9 and 6.1 ng/ml depending on the animal) immediately after DXM injection; this peak was followed by a decrease to low values (0.25 to 0.5 ng/ml) as soon as 4 hours after injection. It is concluded that DXM suppresses the testosterone secretion. Since we observed a large decrease of LH, we postulate that DXM lowers LH release and therefore indirectly lowers the T synthesis and/or release.

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    • "The cortisol:DHEA ratio was also highly correlated with the expression of several inflammatory neutrophil genes in a related study (Buckham Sporer et al., 2008), indicating that these steroid hormones may support a proinflammatory state after transportation of cattle. Elevations in glucocorticoids may drive an attenuation in other circulating steroid hormones (Thibier and Rolland, 1976; Welsh et al., 1979), which is supported in the current study by changes in testosterone and progesterone concentrations . Bulls have been found to have lesser serum cortisol concentrations during transportation than steers (Tennessen et al., 1984), thus, it may be interesting to monitor these other gonadal steroid hormones in steers "
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    ABSTRACT: Transportation causes stress in cattle that may alter numerous physiological variables with a negative impact on production and health. The objectives of the current study were to investigate the physiological effects of truck transportation and to characterize a pattern of phenotypes in the circulation that may aid in the early identification of stress-susceptible animals that often succumb to severe respiratory disease. Thirty-six young beef bulls (Aberdeen Angus, n = 12; Friesian, n = 12; and Belgian Blue x Friesian, n = 12) were subjected to a 9-h truck transportation by road. Blood (10 mL) was collected at -24, 0, 4.5, 9.75, 14.25, 24, and 48 h relative to the initiation of transportation (0 h). Plasma was collected for the assay of various metabolic, inflammatory, and steroid variables, and total leukocyte counts were determined in whole blood at each time point. Body weight and rectal temperature were recorded at -24, 9.75, and 48 h. Transportation decreased measures of protein metabolism in the plasma, including albumin (P = 0.002), globulin (P < 0.001), urea (P = 0.006), and total protein (P < 0.001), and increased creatine kinase (P < 0.001). The energy substrate beta-hydroxybutyrate was not changed (P = 0.27). Acute phase proteins haptoglobin and fibrinogen were both decreased (P < 0.001), whereas total leukocyte counts were elevated (P = 0.002). Circulating steroid concentrations were altered, because a classical acute increase in plasma cortisol was observed with the onset of transit (P < 0.001), in association with a decrease in dehydroepiandrosterone (P = 0.07), resulting in a profound increase in cortisol:dehydroepiandrosterone ratio (P < 0.001). Plasma testosterone was decreased, whereas plasma progesterone was increased (P < 0.001) in association with the increase in cortisol (P < 0.001). There was also an effect of breed for all variables except plasma urea, creatine kinase, and testosterone, perhaps indicating that a genetic component contributed to the physiological response to transportation stress, although without any clear trend. Taken together, this profile of physiological variables in the circulation of transportation-stressed bulls may aid in the future detection of disease-susceptible cattle after transportation. Further research to validate these potential biomarkers is necessary.
    Full-text · Article · Jun 2008 · Journal of Animal Science
    • "Although prior reports demonstrate that glucocorticoids reduce circulating gonadotropin levels[21,29,75,82,88,90], fundamental questions regarding the physiological relevance and mechanism of this suppression remained unanswered when we launched this series of experiments. First, does an acute, physiologic stress-like increase in cortisol , the major glucocorticoid in sheep, suppress LH secretion? "
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    ABSTRACT: This review highlights our recent work investigating the inhibitory effects of acute, physiologic stress-like increases in cortisol on reproductive neuroendocrine activity in sheep, the mechanisms responsible for this suppression, and the relevance of enhanced glucocorticoid secretion to stress-induced inhibition of gonadotropin secretion in this species. Initial studies established that cortisol rapidly suppresses pulsatile luteinizing hormone secretion. In ovariectomized ewes, this inhibition reflects the reduction of pituitary responsiveness to gonadotropin-releasing hormone mediated by the type II glucocorticoid receptor, rather than the suppression in hypothalamic gonadotropin-releasing hormone release. Studies in ovary-intact ewes, however, uncovered an alternative mode of cortisol action. During the follicular phase of the estrous cycle, cortisol reduces luteinizing hormone pulse frequency, most likely via the inhibition of gonadotropin-releasing hormone pulsatility. Recent preliminary evidence in ovariectomized ewes demonstrates increased cortisol secretion is essential for disruption of pulsatile luteinizing hormone secretion in response to a psychosocial stress. Taken together, our observations reveal diverse inhibitory actions of cortisol on gonadotropin secretion and that this glucocorticoid is not only sufficient, but necessary for suppression of reproductive neuroendocrine activity in response to certain types of stress.
    No preview · Article · Aug 2006 · Frontiers in Neuroendocrinology
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    • "Another alternative to consider is that corticosteroids may act to suppress testosterone under normal endogenous regulation, but under conditions of maximal LH stimulation the suppressing effect of corticosteroids may be overcome. Most previous evidence indicates that pituitary suppression as well as decreased testicular steroidogenesis results from adminstration of adrenal corticosteroids (Doerr and Pirke, 1976; Thibier and Rolland, 1976; Chantaraprateep and Thibier, 1978; Welsh et al., 1979). Specific glucocorticoid receptors have been identified in rat interstitial cells (Evain et al., 1976), however, dexamethasone did not block human chorionic gonadotropin (hCG) stimulation of testosterone production by these cells in culture in that study. "
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    ABSTRACT: The effect of adrenocorticotropin hormone (ACTH) on plasma cortisol and on gonadotropin releasing hormone (GnRH)-induced release of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone was determined in nine Holstein bulls and 12 Holstein steers. Treatments consisted of animals receiving either GnRH (200 micrograms, Group G), ACTH (.45 IU/kg BW, Group A) or a combination of ACTH followed 2 h later by GnRH (Group AG). Group G steers and bulls had elevated plasma LH and FSH within .5 h after GnRH injection and plasma testosterone was increased by 1 h after GnRH injection in bulls. In Group A, plasma cortisol was elevated by .5 h after ACTH injection in both steers and bulls, but plasma LH and FSH were unaffected. In Group A bulls, testosterone was reduced after ACTH injection. In Group AG, ACTH caused an immediate increase in plasma cortisol in both steers and bulls, but did not affect the increase in either plasma LH or FSH in response to GnRH in steers. In Group AG bulls, ACTH did not prevent an increase in either plasma LH, FSH or testosterone in response to GnRH compared with basal concentrations. However, magnitude of systemic FSH response was reduced compared with response in Group G bulls, but plasma LH and testosterone were not reduced. The results indicate that ACTH caused an increase in plasma cortisol, but did not adversely affect LH or FSH response to GnRH in steers and bulls. Further, while testosterone was decreased after ACTH alone, neither ACTH nor resulting increased plasma cortisol resulted in decreased testosterone production in the bull after GnRH stimulation.
    Preview · Article · Feb 1983 · Journal of Animal Science
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