scholarly journals Acute and chronic effects of exercise on tissue sensitivity to glucocorticoids

2003 ◽  
Vol 94 (3) ◽  
pp. 869-875 ◽  
Author(s):  
M. Duclos ◽  
C. Gouarne ◽  
D. Bonnemaison
Keyword(s):  
Acute Exercise ◽  
Prolonged Exercise ◽  
The Body ◽  
Adrenal Axis ◽  
Chronic Effects ◽  
Tissue Sensitivity ◽  
Exercise Induced ◽  
Acute And Chronic Effects ◽  
Pituitary Adrenal Axis

The aim of this study was to address the effect of endurance training on tissue sensitivity to glucocorticoids (GC) in both resting and exercising conditions. In vitro dexamethasone inhibition of LPS-induced interleukin-6 secretion in cultures of peripheral monocytes was compared in untrained subjects (UT) and in endurance-trained men (ET) at the end of a 2-h run and during exercise recovery. We demonstrated an in vitro plasticity of sensitivity of monocytes to GC in ET men, superimposed to changes in systemic cortisol concentrations (plasma and saliva). Compared with sedentary men, similar resting cortisol levels in ET men are associated with decreased sensitivity of monocytes to GC 8 and 24 h after the end of the last training session ( P < 0.05, ET vs. UT). Moreover, in these ET subjects, an acute bout of exercise increased the sensitivity of monocytes to GC (at 1000 and 1200; ET vs. UT, P > 0.05). This acute exercise-induced increase in tissue sensitivity to GC, which is synchronous with activation of the hypothalamo-pituitary adrenal axis, may act to shut off muscle inflammatory reaction and cytokine synthesis and then decrease exercise-induced muscle damage or inflammatory response. By contrast, the decreased sensitivity of monocytes to GC reported in ET men 24 h after the last bout of exercise may be related to the process of desensitization that may act to protect the body from prolonged, exercise-induced cortisol secretion. These acute and chronic effects of exercise on tissue sensitivity to GC demonstrate an adaptation of the hypothalamo-pituitary adrenal axis to repeated and prolonged exercise-induced increases in GC secretion.

scholarly journals Acyloxyacyl hydrolase modulates depressive-like behaviors through aryl hydrocarbon receptor

2019 ◽  
Vol 317 (2) ◽  
pp. R289-R300 ◽  
Author(s):  
Lizath M. Aguiniga ◽  
Wenbin Yang ◽  
Ryan E. Yaggie ◽  
Anthony J. Schaeffer ◽  
David J. Klumpp ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Therapeutic Target ◽  
Binding Sites ◽  
Hypothalamic Pituitary Adrenal ◽  
Adrenal Axis ◽  
Aryl Hydrocarbon ◽  
Acyloxyacyl Hydrolase ◽  
Deficient Mice ◽  
Pituitary Adrenal Axis

Corticotropin-releasing factor (CRF) regulates stress responses, and aberrant CRF signals are associated with depressive disorders. Crf expression is responsive to arachidonic acid (AA), where CRF is released from the hypothalamic paraventricular nucleus (PVN) to initiate the hypothalamic-pituitary-adrenal axis, culminating in glucocorticoid stress hormone release. Despite this biological and clinical significance, Crf regulation is unclear. Here, we report that acyloxyacyl hydrolase, encoded by Aoah, is expressed in the PVN, and Aoah regulates Crf through the aryl hydrocarbon receptor (AhR). We previously showed that AOAH-deficient mice mimicked interstitial cystitis/bladder pain syndrome, a condition frequently associated with comorbid anxiety and depression. With the use of novelty-suppressed feeding and sucrose preference assays to quantify rodent correlates of anxiety/depression, AOAH-deficient mice exhibited depressive behaviors. AOAH-deficient mice also had increased CNS AA, increased Crf expression in the PVN, and elevated serum corticosterone, consistent with dysfunction of the hypothalamic-pituitary-adrenal axis. The human Crf promoter has putative binding sites for AhR and peroxisome proliferator-activated receptor (PPARγ). PPARγ did not affect AA-dependent Crf expression in vitro, and conditional Pparγ knockout did not alter the AOAH-deficient depressive phenotype, despite previous studies implicating PPARγ as a therapeutic target for depression. In contrast, Crf induction was mediated by AhR binding sites in vitro and increased by AhR overexpression. Furthermore, conditional Ahr knockout rescued the depressive phenotype of AOAH-deficient mice. Finally, an AhR antagonist rescued the AOAH-deficient depressive phenotype. Together, our results demonstrate that Aoah is a novel genetic regulator of Crf mediated through AhR, and AhR is a therapeutic target for depression.

Effects of short- and long-duration hypothyroidism on hypothalamic–pituitary–adrenal axis function in rats: In vitro and in situ studies

Endocrine ◽  
2012 ◽  
Vol 42 (3) ◽  
pp. 684-693 ◽  
Author(s):  
Elizabeth O. Johnson ◽  
Aldo E. Calogero ◽  
Mary Konstandi ◽  
Themis C. Kamilaris ◽  
Sandro La Vignera ◽  
...  
Keyword(s):  
Hypothalamic Pituitary Adrenal Axis ◽  
Hypothalamic Pituitary Adrenal ◽  
In Situ Studies ◽  
Adrenal Axis ◽  
Long Duration ◽  
Pituitary Adrenal Axis

scholarly journals Effects of mitotane on the hypothalamic–pituitary–adrenal axis in patients with adrenocortical carcinoma

2017 ◽  
Vol 177 (4) ◽  
pp. 361-367 ◽  
Author(s):  
Giuseppe Reimondo ◽  
Soraya Puglisi ◽  
Barbara Zaggia ◽  
Vittoria Basile ◽  
Laura Saba ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Close Correlation ◽  
Inhibitory Effect ◽  
Hypothalamic Pituitary Adrenal Axis ◽  
Adrenocortical Cancer ◽  
Hypothalamic Pituitary Adrenal ◽  
Adrenal Axis ◽  
Direct Inhibitory Effect ◽  
Pituitary Adrenal Axis

Objective Mitotane, a drug used to treat adrenocortical cancer (ACC), inhibits multiple enzymatic steps of adrenocortical steroid biosynthesis, potentially causing adrenal insufficiency. Recent studies in vitro have also documented a direct inhibitory effect of mitotane at the pituitary level. The present study was aimed to assess the hypothalamic–pituitary–adrenal axis in patients with ACC receiving mitotane. Design and methods We prospectively enrolled 16 patients on adjuvant treatment with mitotane after radical surgical resection of ACC, who underwent standard hormone evaluation and h-CRH stimulation. A group of 10 patients with primary adrenal insufficiency (PAI) served as controls for the CRH test. Results We demonstrated a close correlation between cortisol-binding globulin (CBG) and plasma mitotane levels, and a non-significant trend between mitotane dose and either serum or salivary cortisol in ACC patients. We did not find any correlation between the dose of cortisone acetate and either ACTH or cortisol levels. ACTH levels were significantly higher in patients with PAI than that in patients with ACC, both in baseline conditions (88.99 (11.04–275.00) vs 24.53 (6.16–121.88) pmol/L, P = 0.031) and following CRH (158.40 (34.32–275.00) vs 67.43 (8.8–179.52) pmol/L P = 0.016). Conclusions The observation of lower ACTH levels in patients with ACC than that in patients with PAI, both in basal conditions and after CRH stimulation, suggests that mitotane may play an inhibitory effect on ACTH secretion at the pituitary levels. In conclusion, the present study shows that mitotane affects the HPA axis at multiple levels and no single biomarker may be used for the assessment of adrenal insufficiency.

The Hypothalamic Melanocortin System Stimulates the Hypothalamo-Pituitary-Adrenal Axis in vitro and in vivo in Male Rats

2002 ◽  
Vol 75 (4) ◽  
pp. 209-216 ◽  
Author(s):  
Waljit S. Dhillo ◽  
Caroline J. Small ◽  
Leighton J. Seal ◽  
Min-Seon Kim ◽  
Sarah A. Stanley ◽  
...  
Keyword(s):  
Male Rats ◽  
Melanocortin System ◽  
Adrenal Axis ◽  
Pituitary Adrenal Axis

Reproductive and pituitary-adrenal axis parameters in normal and prenatally stressed prepubertal blue foxes (Alopex lagopus)

2003 ◽  
Vol 76 (3) ◽  
pp. 413-420 ◽  
Author(s):  
L. V. Osadchuk ◽  
B. O. Braastad ◽  
A. L. Hovland ◽  
M. Bakken
Keyword(s):  
Stress Responses ◽  
Prenatal Stress ◽  
Plasma Concentrations ◽  
Female Offspring ◽  
Alopex Lagopus ◽  
Adrenal Axis ◽  
Prenatally Stressed ◽  
Blue Fox ◽  
Pituitary Adrenal Axis

AbstractMan-animal relationships are involved in the process of fox domestication. Handling being an important part of man-animal contacts, causes stress responses in farm-bred blue foxes. The purpose of this study was to determine how prenatal stress induced by handling pregnant vixens influences certain morphometric and hormonal parameters of adrenocortical and gonadal function in the prepubertal offspring. Blue fox females were subjected to daily handling sessions, each of 1 min, in the last trimester of pregnancy (term = 52 days). Plasma concentrations of ACTH, cortisol, progesterone, oestradiol and testosterone, as well as the in vitro adrenal and gonadal production of steroids were measured by radio-immunoassay in control (C, no. = 56) and prenatally stressed (PS, no. = 56) blue fox cubs of both sexes at the age of 6 to 7 months. Prenatal stress decreased plasma concentration of cortisol (C: 31·0 (s.e. 4·3) v. PS: 22·7(s.e. 1·6) ng/ml, P < 0·05) as well as progesterone (C: 1·00(s.e. 0·10) v. PS: 0·65(s.e. 0·05) ng/ml, P < 0·05) in female cubs. Prenatal stress did not cause any changes in adrenal or gonadal weights, plasma concentrations of testosterone or oestradiol, or in vitro adrenal or gonadal steroid production, in either sex. It is concluded that persistent handling of pregnant blue foxes did not affect the prepubertal development of the reproductive system but resulted in disregulation in the hypothalamic-pituitary-adrenal axis in the female offspring.

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