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Results for “Adrenocortical Hyperfunction”

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PubMed1987

Effects of synacthen on lipid metabolism in the perfused epididymal fat pad of the rat.

Rats were treated with Synacthen, a synthetic corticotrophin analogue, to induce hypercorticism. The epididymal fat pad was selectively cannulated and perfused. In fasted rats acetone ether powder lipoprotein lipase (LPL) activity rose during treatment to levels found in fed controls. In fed animals no further rise in LPL activity was observed during Synacthen treatment. However, the heparin-elutable LPL activity did not change during this treatment in fasted nor fed animals. Pharmacologic levels of insulin in the perfusion medium caused an increase in heparin-releasable LPL activity as a percentage of total fat pad LPL activity (15% v 48%). Hydrolysis of chylomicrons was higher in fasted three days treated animals then in controls (10 +/- 4% v 2 +/- 2%). In this group a higher uptake of liberated free fatty acids was found (2.6 +/- 1.5% v 1.0 +/- 0.5% in controls). The increase in hydrolysis rate and uptake of fatty acids in the treated fasted animals could not be explained by an increase in releasable LPL activity. Fatty acid release from the fat pad was lower in treated animals than in controls (fasted and fed), basally as well as after adrenalin stimulation. The observation that the epididymal fat pad retains its weight during hypercorticism may therefore be ascribed to an increased influx of fatty acids from increased hydrolysis of TG-rich particles and to an inhibited efflux of fatty acids from the adipocyte. The discrepancy between the LPL activity extractable from an acetone ether powder and the heparin releasable LPL activity suggests impairment of the transport of LPL from the adipocyte to the heparin releasable pool at the endothelium.

Adipose Tissue↗
PubMed1993

The ovine corticotropin-releasing hormone-stimulation test in type I diabetic patients and controls: suggestion of mild chronic hypercortisolism.

We examined hypothalamic-pituitary-adrenal (HPA) axis function in insulin-dependent diabetic outpatients (N = 22) and age-, sex-, and weight-matched normal controls (N = 22). The evaluation included measurements of 9:00 AM fasting plasma cortisol and cortisol-binding globulin (CBG) levels, 24-hour urinary free cortisol (UFC) excretion, and plasma corticotropin and cortisol responses to intravenously administered ovine corticotropin-releasing hormone ([CRH] 1 microgram/kg given as a bolus at 8:00 PM). Diabetic patients had significantly elevated 9:00 AM plasma cortisol levels (mean +/- SE, 300.7 +/- 99.3 v 237.3 +/- 99.3 nmol/L, P < .04), higher 24-hour UFC excretion (313.2 +/- 112.6 v 244.2 +/- 69.3 nmol/24 h, P < .02), and greater cortisol responses to CRH infusion (time-integrated values: 49,408.2 +/- 11,289.8 v 40,217.9 +/- 7,228.6 nmol/L.120 min, P < .004; peak cortisol values: 529.7 +/- 107.6 v 438.7 +/- 77.3 nmol/L, P < .002) than controls. UFC excretion values were positively correlated with both 5-year averaged hemoglobin A1c level (P = .03) and total number of insulin units administered per day (P = .03). These results suggest that insulin-dependent diabetic outpatients have mild chronic hypercortisolism, which might influence the control of the disease and play a role in the development of its chronic complications.

Adrenocortical Hyperfunction↗
PubMed1985

Post-weaning crowding induces corticoadrenal hyperreactivity in male mice.

The effect of various population densities on corticoadrenal function was studied in prepuberal male mice. High population densities decreased body weight gain. Neither adrenal weight nor basal serum corticosterone were modified by crowding. However, corticoadrenal response to some acute stresses such as noise and forced swimming was higher in crowded mice. As corticoadrenal response to adrenocorticotropin remained unaffected, it appears that crowding induced pituitary-adrenal hyperreactivity. Neither the defecation rate nor exploratory activity were altered by crowding, suggesting a dissociation between pituitary-adrenal responsiveness and behavioral measures presumably related to emotional arousal. These discrepancies may possibly be due to the higher sensitivity of corticoadrenal function to environmental changes. Our results suggest that crowding would be suitable as a model for chronic continuous stress.

Acute Disease↗
PubMed1991

Epidermal dexamethasone receptors in dogs with confirmed hyperadrenocorticalism, hypothyroidism or undiagnosed hormonal alopecia.

Low capacity, high affinity [3H] dexamethasone binding receptors were identified in cytosolic preparations of the skin (mean number 42.0 +/- 25.2 fmol mg-1 protein, apparent dissociation constant (1 nM +/- 0.23) of clinically normal dogs. No [3H] dexamethasone binding was observed in the skin of nine out of 10 dogs with confirmed spontaneous hyperadrenocorticism or in the skin of three out of six dogs with undiagnosed hormonal alopecia. A reduction was detected in the number of [3H] dexamethasone binding receptors in the skin of one dog with confirmed hypothyroidism. This study provides evidence for the susceptibility of canine glucocorticoid receptors to down regulation by imbalances of endogenous hormones, particularly increased glucocorticoid concentrations.

Adrenocortical Hyperfunction↗
PubMed1994

Urinary concentration of corticoids in normal horses and horses with hyperadrenocorticism.

The urinary corticoid:creatinine (c:c) ratio was determined in eight horses with hyperadrenocorticism (HAC). The mean (+/- SD) urinary c:c ratio of the eight horses with HAC (29 +/- 14 x 10(-6)) was significantly (P < 0.05) greater than the ratio in seven control horses (11 +/- 4.3 x 10(-6)). The urinary concentration of corticoids in control horses (201 +/- 60.4 nmol litre-1) was significantly (P < 0.05) lower than in horses with HAC (664 +/- 291 nmol litre-1). The urinary creatinine concentrations did not differ significantly (P > 0.05) between both groups. As both false negative and false positive cases were found, it is concluded that a measurement of the urinary c:c ratio in the horse should not be used as the sole test to confirm equine HAC.

Adrenal Cortex Hormones↗
PubMed1975

Postpuberal castration and prostatic carcinoma.

The occurrence of prostatic carcinoma after postpuberal castration is rather unique since only one other case has been reported. However, there was no lack of androgens in the patient in this report, because the testicular ablation was compensated by nodular hyperplasia of the adrenal cortex maintaining a normal plasma testosterone.

Adenocarcinoma↗
PubMed1985

Ontogeny of vasoactive intestinal peptide and somatostatin in different structures of the rat brain: effects of hypo- and hypercorticism.

The ontogeny of the vasoactive intestinal peptide (VIP) and somatostatin (SRIF) was studied in various structures of the rat central nervous system (CNS), using specific radioimmunoassays. The effect of adrenal corticoids on the concentration of both peptides was investigated during the development of the rat from 3 days before birth to 2 months after birth. The evolution of both peptides was different since SRIF was found before birth in each structure tested while VIP appeared only after birth in the same structures. However, after birth the ontogeny of VIP and SRIF was quite similar and the maximum concentration of both peptides occurred between day 14 and day 21. Hypercorticism (implant of corticosterone) and hypocorticism (Metyrapone injections) modified the postnatal evolution of both peptides, suggesting that corticoids play an important role in the brain developmental patterns of VIP and SRIF.

Adrenal Insufficiency↗
PubMed1996

[Food-dependent Cushing syndrome: a new entity of organic hypercorticism].

Diagnosis of Cushing's syndrome is quite difficult in endocrinology. Spontaneous Cushing's syndrome is usually divided into two subgroups, one which is dependent on corticotropin (ACTH) and another one which is not. In the first class are Cushing's disease, the ectopic corticotropin syndrome and the rare ectopic corticotropin-releasing hormone (CRH) syndrome; these ACTH-dependent Cushing's syndrome have usually diffusely enlarged adrenal glands. In the second class are cortisol producing unilateral adrenocortical adenomas or carcinomas, and the recent Cushing's syndrome with food dependent periodic hormonogenesis. This food dependent Cushing's syndrome is an ACTH-independent Cushing's syndrome with multinodular enlargement of both adrenal glands. Pathogenesis is an aberrant adrenal sensitivity to physiologic secretion of gastric inhibitory peptide (GIP). Ectopic expression of GIP receptors on adrenal cells involve pathologic food induced cortisol secretion. Food dependent Cushing's syndrome is a new cause of Cushing's syndrome. Food induced cortisol secretion may have to be explored in the ACTH-independent Cushing's syndrome.

Adrenocortical Hyperfunction↗
PubMed1976

Effects of 25-hydroxycholesterol and aminoglutethimide in isolated rat adrenal cells. A model for congenital lipoid adrenal hyperplasia?

The production of corticosterone from 25-hydroxycholesterol by isolated rat adrenal cells is inhibited by aminoglutethimide phosphate (AGI); half-maximal inhibition is obtained at ca. 10 muM. AGI also inhibits ACTH-stimulated steroid production from endogeneous substrates; here half-maximal inhibition is obtained with ca. 40 muM AGI. In the presence of ACTH + AGI, 25-hydroxycholesterol causes additive inhibition. This effect of 25-hydroxycholesterol is dose-dependent. ACTH-stimulated steroid production from endogeneous substrates is partially inhibited by 5-cholene-3 beta,24-diol. These results may just reflect substrate competition for the side-chain cleaving system or may be due to some seocndary toxic effect on the cells.

Adrenal Glands↗