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Top of pageINTRODUCTIONSubstantial evidence suggests that reproductive steroids modulate the response to stress. This journal is a member of and subscribes to the principles of the Committee on Publication Ethics.
Xenical helps you to achieve weight loss without suppressing your appetite.It is one of the most successful treatment for weight loss. We assessed this role by performing CRH stimulation tests in 10 men (ages 18–45 years) during gonadal suppression with leuprolide acetate and during testosterone addition to leuprolide. Androgen inhibits the increases in hypothalamic corticotropin-releasing hormone (CRH) and CRH-immunoreactivity following gonadectomy. As the first observations of sex differences showed increased HPA axis activity in female rodents, most attention has focused on the effects of estradiol, with little attention paid to the possible modulatory role of testosterone. The pituitary–adrenal response to novel stimulation and ether stress in young adult and aged rats.
Da€™une par la L-thyroxine (L-T4), qui est la plus connue et da€™autre part la€™hormone dont nous venons de parler, la L-triodthyronine (L-T3).
Sexual dimorphisms (largely age-dependent) in stimulated HPA axis activity have been variably reported in humans (Greenspan et al, 1993; Seeman et al, 2001), but there are virtually no studies identifying the role, if any, of androgens in the reported human dimorphisms. A mixed effects regression model showed that testosterone but not estradiol or CBG significantly contributed to the variance of cortisol.
Indeed, in one of few studies evaluating the impact of reproductive manipulation on the HPA axis in men, estrogen was administered and observed to increase the hormonal response to psychosocial stress (Kirschbaum et al, 1996), similar to results in non-human male primates (Norman et al, 1992). Chronic estrogen-induced alterations in adrenocorticotropin and corticosterone secretion, and glucocorticoid receptor-mediated functions in female rats. These data demonstrate that testosterone regulates CRH-stimulated HPA axis activity in men, with the divergent effects on ACTH and cortisol suggesting a peripheral (adrenal) locus for the suppressive effects on cortisol. Thus, the effects of testosterone on the HPA axis in human males are unknown and limited to speculations based on observed sexual dimorphisms in lower animals. All men were aged between 18 and 45 years, were without current medical illness (as assessed by medical history, physical examination, laboratory tests, and EKG), were medication free, and had no history of psychiatric disorders, including alcohol and substance abuse, as determined by the Structured Clinical Interview for DSM III-R or IV (SCID-IIIR or IV) (First et al, 1996).
The protocol was reviewed and approved by the National Institute of Mental Health (NIMH) Institutional Review Board, and all subjects gave both written and verbal consent to study participation.
Following 1 month of leuprolide acetate alone, men were randomly assigned to receive add-back of either 200 mg IM testosterone enanthate or sesame oil injections every 2 weeks for a month in a double-blind, crossover design. The ovine-CRH study was performed 1–12 days after the second injection of testosterone or placebo.
Estradiol was measured by RIA after extraction with LH20 column chromatography in a modification of the procedure by Wu and Lundy (1971). The ACTH-immunoradiometric assay uses paired monoclonal and polyclonal antibodies, reactive, respectively, with the N terminal and the C terminal regions of ACTH.
Opposing effects of androgen and estrogen on pituitary–adrenal function in nonpregnant primates. Baseline measures of HPA axis function (cortisol, ACTH, CBG, UFC) also were compared across hormonal conditions with paired t-tests. Differences in CRH-stimulated ACTH and cortisol levels were assessed with analysis of variance with repeated measures (ANOVA-R), with hormonal condition (testosterone vs placebo replaced) and time (nine levels included the average of the pre-CRH values and each of the post-CRH values) as within subjects variables. As each subject had 18 data points (nine time points in each of two conditions), ANOVA-R (Systat; Port Richmond, CA) was employed as the primary statistical comparison because it takes maximal advantage of all of the data collected, unlike summary measures (eg, area under the curve (AUC), which may not discriminate between differences in the shape of the response curve). Androgen regulation of adrenocorticotropin and corticosterone secretion in the male rat following novelty and foot shock stressors.
Bonferroni corrected post hoc comparisons were performed when the results of the ANOVA-R were significant. Patterns of ACTH and cortisol pulsatility over twenty-four hours in normal males and females. To further estimate the relative contributions of testosterone, estradiol, and CBG to the variance of CRH-stimulated cortisol and ACTH levels across hormonal conditions, a mixed effects regression analysis was performed with SAS Proc Mix (Cary, NC) with the following factors included in the predictive model: hormone condition, time, testosterone, estradiol, CBG.

Sex-specific effects of social support of cortisol and subjective responses to acute psychological stress. UFC did not differ between the induced hormonal conditions (although complete paired collections were obtained in only seven subjects). Short-term estradiol treatment enhances pituitary–adrenal axis and sympathetic responses to psychosocial stress in healthy young men. While there was a trend for the ACTH MAX to be increased during testosterone replacement (p=0.06), no differences were seen in the MAX or AUC.
No condition by time interactions were observed for either CRH-stimulated cortisol or ACTH. Changes in cortisol and ACTH AUC, MAX, and MAX from the hypogonadal to testosterone replaced condition were not significantly correlated with changes across conditions in testosterone, estradiol, CBG, or the ratio of testosterone to estradiol. Pituitary–adrenal function in the rat after gonadectomy and gonadal hormone replacement. A mixed effects regression model examined the contributions of testosterone, estradiol, and CBG, alone and in combination, to the variance of stimulated cortisol and ACTH.
Effects of estrogen and estrous cycle on glucocorticoid and catecholamine responses to stress in sheep. No individual effects were seen for CBG or estradiol, and a trend was seen for a significant contribution of testosterone to the variance of cortisol (over time and across conditions). HPA axis responses to laboratory psychosocial stress in healthy elderly adults, younger adults, and children: impact of age and gender.
Temporal changes in plasma adrenocorticotropin concentration after repeated neurotropic stress in male and female rats. In contrast, our data demonstrate that the effect of testosterone in young men is to inhibit rather than augment the cortisol response to CRH stimulation. Compared with the leuprolide-induced hypogonadal state, testosterone replacement produced a blunted cortisol response, decreased AUC, as well as decreased cortisol MAX and MAX. The effect of ether stress on ACTH and corticosterone in intact, gonadectomized, and testosterone- or estradiol-replaced rats. These findings are consistent with studies in rodents revealing a suppressive rather than enhancing effect of testosterone on stimulated HPA axis activity (Handa et al, 1994; Bingaman et al, 1994). Androgen inhibits, while oestrogen enhances, restraint-induced activation of neuropeptide neurones in the paraventricular nucleus of the hypothalamus. The surprising finding in our study of increased ACTH during testosterone replacement, however, localizes the suppressive effects on cortisol to the periphery.A possible explanation for reduced stimulated cortisol in the face of increased ACTH is decreased adrenal sensitivity.
The present data would suggest even greater modulation of adrenal sensitivity by testosterone, as not only is ACTH significantly higher but cortisol is also significantly lower compared with the hypogonadal state. Peripheral and central sex steroids have differential effects on the HPA axis of male and female rats.
The effect of testosterone on cortisol, however, appears to be confined to stimulated levels, as no difference in either basal cortisol or UFC was observed across the induced hormonal conditions. Using dispersed inner adrenocortical cells, Nowak et al (1995) showed that testosterone inhibited ACTH-stimulated but not basal corticosterone output in vitro. Stalvey (2002) similarly demonstrated a reduction by testosterone of 3HSD activity, immunoreactivity, and m-RNA in cultured mouse adrenal cells under both basal and stimulated conditions. The effects of gonadectomy and sex hormones on plasma ACTH and on the reactivity of the anterior pituitary gland to CRF. The restriction of the effects of testosterone in the current results to (ACTH) stimulated rather than basal conditions (Nowak et al, 1995) suggests that testosterone may interfere with ACTH signaling at the adrenal.
While testosterone-related decreases in ACTH bioactivity have been observed in vitro (Coyne and Kitay, 1969), the resultant decrease in cortisol would be expected under basal conditions, which was not observed in this study.Downstream effects of the removal and administration of testosterone may have contributed to the results observed in this study. Exposure to ovarian steroids elicits a female pattern of plasma cortisol levels in castrated male macaques. Testosterone replacement was associated with significant increases in estradiol (393%) and decreases in CBG (18%).

While decreased CBG could account for lower stimulated cortisol values during testosterone administration, the changes in CBG across hormonal conditions were not significantly correlated with changes in the summary measures of HPA axis function (AUC, MAX, MAX); further, the mixed effects regression analysis demonstrated that CBG did not account for a significant portion of the variance of stimulated cortisol or ACTH when testosterone and estradiol were included in the model. Effects of sex hormones on the steroidogenic activity of dispersed adrenocortical cells of the rat adrenal cortex.
We observed a significant negative correlation between the increase in estradiol (but not testosterone) and the decrease in cortisol AUC from the hypogonadal to the testosterone replaced condition. The consequent suggestion that testosterone inhibition of stimulated cortisol is mediated by the testosterone metabolite estradiol is contradicted by several factors. Gonadal steroids exert facilitating and 'buffering' effects on glucocorticoid-mediated transcriptional regulation of corticotropin-releasing hormone and corticosteroid receptor genes in rat brain.
Second, consistent with this possibility (and more immediately relevant) is the demonstration by Kirschbaum et al (1996) of increased cognitive stress-stimulated cortisol (and ACTH) secretion during short-term estradiol administration to young men; increased mean plasma cortisol concentrations during estradiol administration were also observed in castrated male macaques (Norman et al, 1992).
Hormonal regulation of type II glucocorticoid receptor messenger ribonucleic acid in rat brain. Finally, estradiol did not account for a significant part of the variance of stimulated cortisol if testosterone was included in the regression model. Indeed, only testosterone was found to account for a significant part of the variance of stimulated cortisol secretion.The increased stimulated ACTH secretion during testosterone replacement could reflect decreased feedback inhibition or increased corticotroph sensitivity to CRH.
Similarly, a central action of testosterone or estradiol should appear as increased basal ACTH levels and would not be apparent with exogenous CRH stimulation (or would appear as blunting due to CRH receptor downregulation at the corticotroph).As an alternative explanation, the increase in CRH-stimulated ACTH during testosterone replacement could represent the effects of increased levels and activity of vasopressin (AVP) in the paraventricular nucleus (PVN), which would augment the response to endogenous or exogenous CRH. Such an augmentation of AVP by testosterone was postulated by Rubin et al (1999) to explain the increased ACTH response to cholinergic stimulation seen in men compared with women. Testosterone regulates AVP synthesis and receptor activity in several brain regions critical to HPA axis control, including the PVN and medial preoptic area (Viau and Meaney, 1991, 1996; DeVries et al, 1985).
Fast glucocorticoid feedback inhibition of ACTH secretion in the ovariectomized rat: effect of chronic estrogen and progesterone.
Nonetheless, the findings of Viau et al (1999), Viau and Meaney (1996), Patchev and Almeida (1996) and others suggest that the effects of testosterone on AVP (and subsequent effects on ACTH) are complex and differ according to brain region (eg, PVN vs MPOA), paradigm (basal vs stress (type-dependent)-stimulated), gender, and species.
Similar to findings in animal studies, CRH-stimulated cortisol was decreased during testosterone-replaced compared with hypogonadal conditions.
The concomitant increase in ACTH suggests that the decrease in stimulated cortisol levels by testosterone or its metabolites is mediated at the level of the adrenal gland. Notwithstanding the value of the repeated measures design, the sample size is small, and the differences observed across hormonal conditions, while significant, are small in magnitude (particularly the ACTH results) and of unclear clinical significance.
Pituitary–adrenal cortical responses to low-dose physostigmine and arginine vasopressin administration in normal women and men.
Nonetheless, our findings complement our earlier demonstration of the regulatory role of progesterone on the HPA axis in women (Roca et al, 2003) and suggest that, as in animals, the reproductive axis actively participates in the regulation of the stress axis and is not merely acted on by it. While the effects observed in this study are quite modest, they demonstrate that the enhanced stimulated HPA axis activity previously described in young men compared with young women cannot be ascribed to an activational upregulation of the axis by testosterone. Inhibition of 3b-hydroxysteroid dehydrogenase-isomerase in mouse adrenal cells: a direct effect of testosterone.
Sex differences in physiological responses to stress and in coronary heart disease: a causal link? Independent and overlapping effects of corticosterone and testosterone on corticotropin-releasing hormone and arginine vasopressin mRNA expression in the paraventricular nucleus of the hypothalamus and stress-induced adrenocorticotropic hormone release. Effects of estrogen antagonists and agonists on the ACTH response to restraint stress in female rats.

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