The Effect of Glucocorticoids on Corticosteroid Binding Globulin

Schlechte, Janet A.; Hamilton, David

doi:10.1111/j.1365-2265.1987.tb01145.x

Cited by 74 publications

(31 citation statements)

References 24 publications

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“…In rats treated with dexamethasone. a decrease in serum CBG was observed and it was related to diminished CBG mRNA synthesis [23], whereas in adrenalectomized ani mals, CBG production was increased from perfused rat liver [21], These observations suggest that glucocorticoids may modulate CBG production and are consistent with the findings of decreased plasma CBG in Cushing syn drome [24] and in patients receiving glucocorticoids [25], A report on women with polycystic ovary syndrome found a significant reduction in immunoreactivc CBG and the authors speculated that it could be related to increased activity of the adrenal axis [26], Lack of diurnal variations in CBG however does not support the hypothe sis of a regulation of CBG production by glucocorticoids under physiological circumstances.…”

Section: Effects O F Glucocorticoidssupporting

confidence: 79%

Corticosteroid-Binding Globulin during Inflammation and Burn Injury: Nutritional Modulation and Clinical Implications

Garrel¹

1996

Horm Res

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Corticosteroid-binding globulin (CGB) is the main carrier of glucocorticoids in mammals. Serum CBG shows little physiological variation with the exception of pregnancy. Experimental inflammation and burn injury decrease serum CBG in rats and while the mechanism of this effect is unknown, in vitro experiments suggest that interleukin-6 may be involved. In severely burned patients, we have found that CBG was markedly decreased within a few hours postinjury. This decrease lasted about 2 weeks and was accompanied by an increase in the free fraction of serum cortisol. In addition, serum CBG responded to dietary manipulation in these patients, with low fat feeding resulting in higher serum CBG concentrations and lower serum-free cortisol values. This finding suggests that during severe stress, CBG may be important in regulating the amount of cortisol reaching target tissues such as the immune system and wounds.

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Section: Effects O F Glucocorticoidssupporting

confidence: 79%

Corticosteroid-Binding Globulin during Inflammation and Burn Injury: Nutritional Modulation and Clinical Implications

Garrel¹

1996

Horm Res

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“…2) and after the women were split by group (data not shown). We examined the correlation between the two parameters after splitting cortisol values by concentration ranges, excluding from the analysis the post-dexamethasone cortisol values, because of the in¯uence of exogenous glucocorticoids on circulating corticosteroid-binding globulin (CBG) concentrations (25). We found that the correlation was lost for plasma cortisol concentrations greater than 500 nmol/l (Fig.…”

Section: Correlations Between Plasma Salivary and Urinary Cortisolmentioning

confidence: 99%

Salivary cortisol measurement in normal-weight, obese and anorexic women: comparison with plasma cortisol

Putignano

Dubini

Toja

et al. 2001

European Journal of Endocrinology

156

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Objective: To compare salivary, plasma and urinary free cortisol (UFC) measurements in patients with anorexia nervosa, in whom an overdrive of the hypothalamic±pituitary±adrenal (HPA) axis is well established but information on salivary cortisol is lacking, in viscerally obese patients in whom subtle abnormalities of cortisol secretion and metabolism are postulated, and in normal-weight healthy women. Participants and experimental design: Measurement of salivary cortisol offers a convenient way to assess the concentrations of free, biologically active cortisol in plasma in different physiopathological settings. Forty-seven drug-free, newly diagnosed women with active restrictive anorexia nervosa, 30 restrictive anorexic women undergoing chronic psychopharmacological treatment, 47 women with mild-to-moderate visceral obesity, 103 women with severe central obesity and 63 normal-weight healthy women entered the study. Salivary and blood samples were collected at 0800 h, 1700 h and 2400 h, together with three consecutive 24-h urine specimens for UFC determination. In controls and patients with anorexia nervosa n 83Y salivary and plasma cortisol were also measured after a 1-mg overnight dexamethasone suppression test (DST). In patients with anorexia nervosa, mood was rated by the Hamilton scale for anxiety and depression. Results: Untreated patients with anorexia nervosa showed increased plasma and salivary cortisol and UFC concentrations (all P , 0X001 compared with controls), and decreased cortisol suppression after DST in plasma and saliva (P , 0X0001 and P , 0X005 respectively compared with controls). These alterations were less pronounced, although still statistically signi®cant, in treated patients with anorexia nervosa. Salivary cortisol was highly correlated with paired plasma cortisol in the whole population and after splitting the participants by group P , 0X0001X However, for plasma cortisol values greater than 500 nmol/l (the corticosteroid-binding globulin saturation point), this parallelism was lost. Taking plasma cortisol as a reference, the level of agreement for postdexamethasone salivary and plasma cortisol was 58.9% among suppressors and 77.8% among nonsuppressors (x 2 test: P , 0X01). Decreased 0800 h/2400 h cortisol ratios were observed in plasma and saliva in drug-free patients with anorexia nervosa (P , 0X005 and P , 0X05 respectively compared with controls), and in saliva in severely obese patients (P , 0X05 compared with controls). Depression and anxiety scores were unrelated to cortisol concentrations in any compartment. Conclusions: Salivary cortisol measurement is a valuable and convenient alternative to plasma cortisol measurement. It enables demonstration of the overdrive of the HPA axis in anorexia nervosa and subtle perturbations of the cortisol diurnal rhythm in women with visceral obesity. With the establishment of more speci®c and widely acceptable cut-off values for dynamic testing, measurement of salivary cortisol could largely replace plasma cortisol measurement.

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“…108 The production of cortisol in adrenocortical cells in response to ACTH occurs within minutes, and there is a shift towards an increase in glucocorticoid and away from mineralocorticoid and androgen production. 113 The CBG concentration in serum and the CBG binding affinity are both decreased 22,23,26,238 resulting in a dramatic increase in the biological active free cortisol concentration. In addition, the glucocorticoid receptor shows an increased affinity to free hormone during the acute phase of critical illness.…”

Section: Hpa (Dys)function In Human Sepsismentioning

confidence: 99%

Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

Beishuizen

Thijs

2003

Journal of Endotoxin Research

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Endotoxin is considered to be a systemic (immunological) stressor eliciting a prolonged activation of the hypothalamo-pituitary-adrenal (HPA) axis. The HPA-axis response after an endotoxin challenge is mainly due to released cytokines (IL-1, IL-6 and TNF-a) from stimulated peripheral immune cells, which in turn stimulate different levels of the HPA axis. Controversy exists regarding the main locus of action of endotoxin on glucocorticoid secretion, since the effect of endotoxin on this neuro-endocrine axis has been observed in intact animals and after ablation of the hypothalamus; however, a lack of LPS effect has been described at both pituitary and adrenocortical levels. The resulting increase in adrenal glucocorticoids has well-documented inhibitory effects on the inflammatory process and on inflammatory cytokine release. Therefore, immune activation of the adrenal gland by endotoxin is thought to occur by cytokine stimulation of corticosteroidreleasing hormone (CRH) production in the median eminence of the hypothalamus, which, in turn stimulates the secretion of ACTH from the pituitary. Acute administration of endotoxin stimulates ACTH and cortisol secretion and the release of CRH and vasopressin (AVP) in the hypophysial portal blood. During repeated endotoxemia, tolerance of both immune and HPA function develops, with a crucial role for glucocorticoids in the modulation of the HPA axis. A single exposure to a high dose of LPS can induce a long-lasting state of tolerance to a second exposure of LPS, affecting the response of plasma TNF-a and HPA hormones. Although there are gender differences in the HPA response to endotoxin and IL-1, these responses are enhanced by castration and attenuated by androgen and estrogen replacement. Estrogens attenuate the endotoxin-induced stimulation of IL-6, TNF-a and IL-1ra release and subsequent activation in postmenopausal women. There appears to be a temporal and functional relation between the HPA-axis response to endotoxin and nitric oxide formation in the neuro-endocrine hypothalamus, suggesting a stimulatory role for nitric oxide in modulating the HPA response to immune challenges. demonstrate higher plasma levels of IL-1 and TNF-a. Elevation of plasma glucocorticoids results in suppression of cytokines such as IL-1, IL-6, and TNF-a and in up-regulation of other cytokines, such as IL-4 and IL-10, and cytokine receptors. Thus, by regulation of cytokine production and action, the HPA axis contributes to modulation of the response to inflammation/infection. In addition, the role of HPA activation has been suggested to be a negative feedback system provided by the immunosuppressive activity of glucocorticoids, limiting inflammatory responses and preventing the immune system from over-reacting and causing tissue damage or autoimmunity.As early as 1957, Wexler et al. suggested that LPS could induce ACTH release since they found a depletion of ascorbic acid and cholesterol in the adrenal glands. 10 Moreover, LPS was not able to cause these changes in hypophysectomized rats. ...

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The Effect of Glucocorticoids on Corticosteroid Binding Globulin

Cited by 74 publications

References 24 publications

Corticosteroid-Binding Globulin during Inflammation and Burn Injury: Nutritional Modulation and Clinical Implications

Corticosteroid-Binding Globulin during Inflammation and Burn Injury: Nutritional Modulation and Clinical Implications

Salivary cortisol measurement in normal-weight, obese and anorexic women: comparison with plasma cortisol

Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

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