Plasma Cortisol Response to Insulin and Circadian Rhythm in Diabetic Subjects

Diabetes ◽  
1968 ◽  
Vol 17 (3) ◽  
pp. 124-126 ◽  
Author(s):  
M. Serio ◽  
B. Tarquini ◽  
P. Contini ◽  
A. Bucalossi ◽  
R. Toccafondi
Keyword(s):  
Circadian Rhythm ◽  
Plasma Cortisol ◽  
Cortisol Response

Changes in circadian rhythm and suppression of the plasma cortisol level after prolonged stress in the sheep

1985 ◽  
Vol 110 (4) ◽  
pp. 540-545 ◽  
Author(s):  
F. Przekop ◽  
E. Stupnicka ◽  
E. Wolińska-Witort ◽  
K. Mateusiak ◽  
B. Sadowski ◽  
...  
Keyword(s):  
Circadian Rhythm ◽  
Cortisol Level ◽  
Plasma Cortisol ◽  
Plasma Cortisol Level ◽  
Diurnal Variations ◽  
Cortisol Response ◽  
Time Of Application ◽  
Prolonged Stress ◽  
Similar Decrease ◽  
Stimulation Of

Abstract. Diurnal variations in the plasma cortisol level were studied in anoestrous, pro-oestrous and pregnant ewes subjected to weak electric stimulation of the forelimbs 9 h daily for 3 consecutive days. In non-pregnant ewes the cortisol level rose on each of the 3 days when the stimulation was applied and then decreased on the day following the stimulation. A similar decrease in plasma cortisol concentrations in pregnant ewes appeared on the second day of footshocking. The acrophase of the circadian rhythm on electrostimulation days was synchronous with the time of application of footshocks; therefore, in stimulated ewes it was significantly accelerated compared to the prestimulatory day. A decrease in the plasma cortisol level in pro-oestrous and pregnant ewes was accompanied by disappearance of its normal rhythmicity. Since a normal plasma cortisol response to exogenous corticotrophin was noted after 3 days of foot-shocking it seems unlikely that the decrease in the cortisol level after prolonged stress was caused by exhaustion of the adrenal cortex. Some central mechanisms which could account for the biphasic changes in the plasma cortisol level and for disturbances of the hormone diurnal rhythmicity under conditions of prolonged stress are discussed.

Biological activity of adrenocorticotropic hormone precursors on ovine adrenal cells

1995 ◽  
Vol 268 (4) ◽  
pp. E623-E629 ◽  
Author(s):  
J. Schwartz ◽  
F. Kleftogiannis ◽  
R. Jacobs ◽  
G. D. Thorburn ◽  
S. R. Crosby ◽  
...  
Keyword(s):  
Biological Activity ◽  
Plasma Cortisol ◽  
Inhibitory Action ◽  
Adrenocorticotropic Hormone ◽  
Physiological Role ◽  
Cortisol Response ◽  
Adrenal Cells ◽  
Fetal Cells ◽  
Fetal Plasma ◽  
Cortisol Responses

Adrenocorticotropic hormone (ACTH) is synthesized in the corticotrophs as a precursor, pro-opiomelanocortin (POMC), which is processed via proACTH to ACTH. Both precursors and ACTH are secreted. Although the steroidogenic activity of ACTH is well characterized, that of the precursors is not. This study assessed the capacity of POMC and proACTH to alter cortisol synthesis. POMC and proACTH were prepared by subjecting medium, conditioned by exposure to DMS-79 cells, to Sephadex chromatography, and the bioactivity was assessed in cultured-dissociated ovine adrenal cells. Alone neither POMC (< or = 2.6 nM) nor proACTH (< or = 0.7 nM) showed any consistent acute (6 h) stimulatory or inhibitory action on cortisol in either fetal or adult cells. In contrast, in fetal cells the precursors inhibited steroidogenic response to ACTH-(1-24). POMC at 2.6 nM, but not lower concentrations, decreased the cortisol responses to 0.01, 0.1, and 1 nM ACTH by at least 50%. ProACTH (0.70 and 0.23 nM) decreased the responses to ACTH at 0.01 nM by 89 and 67%, respectively, and at 0.1 nM by 49 and 34%, respectively. At 1 nM ACTH only 0.7 nM proACTH decreased the response to ACTH (by 69%). In contrast, in adult adrenal cells, the precursors did not significantly reduce the response to ACTH (range 0.01-1 nM). Therefore, these data indicate that POMC and proACTH can inhibit the cortisol response to ACTH in fetal adrenal cells, an effect that is concentration dependent. The data suggest that precursors may play a physiological role, possibly regulating fetal plasma cortisol concentrations.

Autoantibodies reacting with vasopressin and oxytocin in relation to cortisol secretion in major depression

2011 ◽  
Vol 26 (S2) ◽  
pp. 904-904
Author(s):  
F.D. Garcia ◽  
Q. Coquerel ◽  
E. Kiive ◽  
P. Déchelotte ◽  
J. Harro ◽  
...  
Keyword(s):  
Major Depression ◽  
Physical Exercise ◽  
Plasma Levels ◽  
Plasma Cortisol ◽  
Cortisol Response ◽  
Cortisol Secretion ◽  
Mild Depression ◽  
Moderate Depression ◽  
Before And After ◽  
Underlying Mechanisms

IntroductionAbnormal vasopressin (VP) and oxytocin (OT) signaling may contribute to the altered activity of the hypothalamo-pituitary-adrenal (HPA) axis in major depression; the underlying mechanisms remain uncertain.ObjectiveThis study characterized plasma levels and affinities of OT-and VP-reactive autoantibodies (autoAbs) with relation to disease severity and plasma cortisol response to physical exercise in patients with mild and moderate depression and healthy controls.MethodsPhysical exercise was used to elicit plasma cortisol response in 23 male depressive and 20 healthy subjects. All subjects were evaluated by the MADRS. Plasma levels VP-and OT-reactive IgG, IgA and IgM autoAbs were measured by ELISA, before and after the exercise, and affinity was measured by plasmon resonance.ResultsPlasma levels of OT-and VP-reactive total IgG autoAbs were lower in patients with moderate depression vs. controls and patients with mild depression. Both OT- and VP- free IgG autoAbs levels were negatively correlated with MADRS scores. Affinity values displayed 100 fold variability in both groups. Patients with moderate depression displayed blunted response of cortisol secretion to physical exercise. Baseline levels of VP total IgG and IgM autoAbs correlated negatively and of VP free IgG autoAbs correlated positively with plasma cortisol after physical exercise.ConclusionThese data show that changes of levels but not affinity of OT- and VP- reactive autoantibodies can be associated with the altered mood in subjects with moderate depression and that levels of VP-reactive autoAbs are associated with cortisol secretion.

Clinical tests explain blunted cortisol responsiveness but not mild hypercortisolism in amenorrheic runners

1994 ◽  
Vol 76 (3) ◽  
pp. 1302-1309 ◽  
Author(s):  
M. J. De Souza ◽  
A. A. Luciano ◽  
J. C. Arce ◽  
L. M. Demers ◽  
A. B. Loucks
Keyword(s):  
Negative Feedback ◽  
Plasma Cortisol ◽  
Adrenocorticotropic Hormone ◽  
Stimulation Test ◽  
Cortisol Response ◽  
Clinical Tests ◽  
Stimulation Tests ◽  
Cortisol Responses ◽  
Sedentary Women ◽  
Secretory Capacity

To investigate mechanisms of blunted adrenocortical responsiveness to exercise and mild hypercortisolism in amenorrheic runners, adrenocorticotropic hormone [ACTH-(1–24) 0.25 mg Cortrosyn] stimulation tests were performed in the presence and absence of overnight dexamethasone (1 mg) suppression (DX and NDX condition, respectively) in six eumenorrheic sedentary women (ES), nine eumenorrheic runners (ER), and nine amenorrheic runners (AR). Before the NDX stimulation test, plasma cortisol was higher (P < 0.001) in AR than in ER and ES. The cortisol response to the NDX stimulation test was blunted (P < 0.001) in AR but reached similar (P > 0.7) peak levels in all groups. Dexamethasone suppressed (P < 0.001) cortisol to similar (P > 0.5) levels (approximately 20 nmol/l) in all groups. In AR, cortisol responses to the DX test were larger (P < 0.03) than to the NDX test and similar (P > 0.6) in the three groups, again reaching comparable (P > 0.8) peak levels. The blunted cortisol response to stimulation in AR in the presence of their mild hypercortisolism appears to be due to a normal limitation in maximal adrenal secretory capacity. Extrapituitary modulators of adrenal responsiveness to ACTH may explain the mild hypercortisolism observed in AR, but limitations of these tests prevent a central negative-feedback defect or an intrinsic adrenal abnormality from being excluded until results of additional studies with even lower doses of dexamethasone and submaximal doses of ACTH-(1-24) are available.

scholarly journals Tail Docking of Piglets 2: Effects of Meloxicam on the Stress Response to Tail Docking

Animals ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1699
Author(s):  
Rebecca Morrison ◽  
Paul Hemsworth
Keyword(s):  
Stress Response ◽  
Plasma Cortisol ◽  
Acute Stress ◽  
Behavioural Response ◽  
Cortisol Response ◽  
Total Plasma ◽  
Sham Treatment ◽  
Commercial Viability ◽  
Tail Docking ◽  
Acute Stress Response

This experiment assessed the efficacy of the cauterisation procedure with or without pain relief (injectable meloxicam) in mitigating the acute stress response to tail docking. Male piglets (n = 432) were allocated to the following treatments at 2-d post-farrowing: (1) no handling, (2) sham handling, (3) tail docked using clippers, (4) tail docked using a cauteriser, (5) meloxicam + clipper, and (6) meloxicam + cauteriser. Meloxicam treatments used Metacam® at 5 mg/mL injected i.m. 1 h prior to tail docking. Blood samples were collected at 15 and 30 min post-treatment and analysed for total plasma cortisol. Behaviours indicative of pain such as escape attempts, vocalisations and standing with head lowered were measured. The duration of vocalisations and frequency of escape attempts during treatment were greater in all tail docking treatments compared to the sham treatment. Piglets in the clipper treatment had higher (p < 0.05) cortisol concentrations at 30 min but not 15 min after treatment and stood for longer (p < 0.001) with head lowered in the first 60 min after treatment than those in the cauterisation treatment. Meloxicam reduced (p < 0.05) both the cortisol response at 30 min after tail docking with the clipper as well as the behavioural response in the first 60 min after tail docking with the clipper. In comparison to the sham treatment, cortisol concentrations at 15 min were higher in the two tail docking treatments whereas the tail docking treatments with meloxicam were similar to the sham handling treatment. In comparison to the sham handling treatment, cortisol concentrations at 30 min post-docking were higher (p < 0.05) only in the clipper treatment. While cauterisation appears to be less aversive than the clipper procedure, the administration of meloxicam did not mitigate the behavioural response during tail docking using either procedure, but reduced standing with head lowered in the first hour after docking for both methods. The commercial viability of administration of meloxicam requires consideration before it is recommended for use compared to cauterisation alone, as it requires additional handling of piglets and costs.

scholarly journals GH and cortisol rebound rise during and following a somatostatin infusion: studies in dogs with the use of a GH-releasing peptide

2002 ◽  
Vol 174 (3) ◽  
pp. 387-394 ◽  
Author(s):  
AE Rigamonti ◽  
SM Bonomo ◽  
SG Cella ◽  
EE Muller
Keyword(s):  
Hpa Axis ◽  
Plasma Cortisol ◽  
Cortisol Response ◽  
Marked Rise ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Combined Administration ◽  
Cortisol Responses ◽  
Plasma Gh

GH-releasing peptides (GHRPs), a class of small synthetic peptide and non-peptide compounds, act on specific receptors at both the pituitary and the hypothalamic level to stimulate GH release in both humans and other animals. GHRPs, like corticotropin-releasing hormone (CRH), also possess acute ACTH- and cortisol-releasing activity, although the mechanisms underlying the stimulatory effect of GHRPs on the hypothalamo-pituitary-adrenal (HPA) axis are still unclear. In recent years, studies in humans and other animals have provided evidence that the rebound GH rise which follows withdrawal of an infusion of somatostatin (SS) (SSIW) is due, at least in part, to the functional activation of GH-releasing hormone (GHRH) neurons of the recipient organism. Unexpectedly, in humans, SS infusion, at a dose inhibiting basal GH secretion, has been associated with an activation of the HPA axis, leading to the hypothesis that this response was mediated, at least in part, by a central nervous system ACTH-releasing mechanism activated by the SS-induced decrease in GH secretion. Interestingly, the rebound GH rise which follows SSIW was magnified by the administration, before SS withdrawal, of a GHRP, implying that the SSIW approach could also be exploited to investigate in vivo the functional interaction in the process of GH and/or ACTH/cortisol secretion between endogenous GHRH (and/or other ACTH-releasing mechanisms) and GHRPs. In the present study, six young beagle dogs were given, on different occasions, at the beginning and at the end of a 3-h i.v. infusion of SS or saline (SAL), a bolus of physiological SAL or a GHRP compound, EP51216. SSIW induced a GH rebound rise without affecting plasma cortisol concentrations, while the withdrawal of SAL infusion was ineffective on either hormone paradigm. Administration of EP51216 at the beginning of SAL infusion evoked release of both GH and cortisol, whereas EP51216 administration at the withdrawal of SAL infusion evoked somatotroph and cortisol responses which were reduced in amplitude and duration. SS infusion significantly reduced the secretion of GH elicited by EP51216 but did not affect the rise of plasma cortisol levels. Interestingly, SSIW resulted in a marked enhancement of the somatotroph and cortisol responses evoked by EP51216. The marked rise of plasma GH levels induced by the GHRP after SSIW recalled that occurring after acute combined administration of recombinant human GHRH and EP51216, implying that exogenously delivered GHRP had synergized with the endogenous GHRH release triggered by SSIW. In contrast, acute combined administration of GHRH and the GHRP induced a cortisol response not different from that induced by GHRP alone, indicating that endogenous GHRH release was not involved in the enhanced cortisol response following EP51216 administration after SSIW. Similarly, the direct involvement of endogenous CRH could be ruled out, since i.v. administration of ovine CRH after SSIW evoked cortisol peak levels not different from those evoked by CRH at the withdrawal of SAL infusion. In conclusion, enhancement of the GH response to EP51216 alone by SSIW, to an extent reminiscent of that following combined administration of GHRH and EP61216, reinforces the view that SSIW elicits release of endogenous GHRH. Further studies are indeed necessary for a better understanding of the mechanisms underlying the enhanced cortisol response, since from now on the involvement of endogenous GHRH or CRH can be ruled out.

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