The effect of dexamethasone (DXM) on circulating testosterone (T) and luteinizing hormone (LH) in young postpubertal bulls;.
ABSTRACT 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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ABSTRACT: Studies of the hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-testicular (HPT) axis have revealed a reciprocal relationship between these two endocrine pathways. In rats, for example, disruption of the HPT axis alters the circadian secretion of corticosterone. Stress, on the other hand, can have varying effects on testosterone secretion in both rats and humans. Furthermore, in contrast to humans, where several pulses of testosterone secretion can be detected across the 24-h period with the largest in the morning, rats appear to exhibit a diurnal rhythm of testosterone secretion. In the present study, we used an automated blood sampling system to investigate the true circadian pattern of testosterone secretion under basal conditions and investigated how this responds to changes in levels of circulating corticosteroids. Analysis of plasma testosterone revealed the expected bimodal pattern of basal testosterone secretion. The two secretory episodes were 12.59 h +/- 41 min apart and 4.04 h +/- 16 min long, with one in the light phase and the other in the dark phase of the cycle. Interestingly, when both testosterone and corticosterone diurnal profile were compared, we found that the circadian rise in plasma corticosterone levels falls neatly between the two testosterone secretory episodes. Treatment of rats with the synthetic glucocorticoid methylprednisolone in their drinking water abolished the normal bimodal profile of testosterone secretion. These rats show transient pulses of testosterone throughout the 24 h, but no circadian pattern. By contrast, adrenalectomised rats maintain their bimodal circadian pattern, suggesting that an intact HPA axis is not necessary for generation of the endogenous HPT rhythm. Thus, although the circadian rhythm of testosterone does not depend on normal HPA function, increased levels of glucocorticoids can abolish normal HPT rhythmicity.Journal of Neuroendocrinology 08/2009; 21(9):737-41. · 3.33 Impact Factor
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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.Journal of Animal Science 06/2008; 86(6):1325-34. · 2.09 Impact Factor
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ABSTRACT: Chronic anxiety, depression and physical exertion-related stress consistently activate the hypothalamic-pituitary-adrenal axis. Almost each component of this activated axis , such as CRH, ACTH, β-endorphin and glucocorticoids exerts profound inhibitory effects on the hy-pothalamic-pituitary-ovarian axis and subsequently leads to reproductive failure in females. The pulsatile secretion of GnRH and the response of gonadotrophs to GnRH stimulation are severely impaired. Increased levels of glucocorticoids moreover inhibit gonadal axis at the hypothalamic, pituitary and ovarian levels and concurrently result in deficient ovarian ster-oidogenesis, amenorrhea, anovulation, defective endometrial decidualization and implanta-tion, abnormal fetal outcome and delayed parturition. Stress-associated growth hormone deficiency with a corresponding deficiency of insulin-like growth factor-1 at the level of the pituitary, ovary and uterine endometrium also leads to de-fective reproductive outcome in females. Moreover, stress-related imbalance between pro-oxidant and antioxidant forces may cause damage to the released ovum, embryo fragmenta-tion, implantation failure or abortion.Biomedical Research. 01/2009; 20:79-83.