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SUMMARY
An investigation was made of the interactions between insulin and cortisol on carbohydrate, fat and protein metabolism in the marsupial brush-tailed opossum Trichosurus vulpecula (Kerr).
Intravenous injection of 0·15 i.u. regular insulin/kg caused a prompt fall in plasma glucose concentration to 33–54% of the control value, in the first 30 min, with complete recovery within 4 h. This was associated with a slow fall in plasma amino acid concentration and a moderate rise in plasma free fatty acid (FFA) concentration. Plasma cortisol concentration was increased 1·5 h after insulin injection to maximum values of 1·24–4·44 μg/100 ml, which were approximately proportional to the degree of hypoglycaemia.
Pretreatment with five daily i.m. injections of 1 mg cortisol acetate/kg caused a marked reduction in insulin sensitivity of three out of four opossums, and increasing the dose to 5 mg/kg caused a similar reduction in insulin sensitivity of the remaining opossum. Cortisol pretreatment raised the control plasma amino acid and FFA concentrations and enhanced the effect of insulin injection on these variables. There was a linear relationship between the control plasma cortisol concentration, within the physiological range, and sensitivity to insulin.
It is concluded that, in contrast to the red kangaroo, the interactions between insulin and glucocorticoids in Trichosurus resemble those reported for eutherian mammals. However, the unusual increase in plasma FFA after insulin injection is unexplained.
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SUMMARY
The major metabolic pathways of cortisol have been studied in detail after injection of a tracer dose of [4-14C]cortisol in two patients with rheumatoid arthritis and in one with disseminated lupus erythematosus. Results are also presented from preliminary experiments in two other patients with rheumatoid arthritis.
The rates of cortisol secretion by the adrenals of all the patients studied were within the normal range and the kinetics of cortisol metabolism were also normal. No abnormalities were found in either the proportions of cortisol, cortisone and 6β-hydroxycortisol in the urinary fraction containing the unconjugated steroids or in that of tetrahydrocortisol, allo-tetrahydrocortisol, tetrahydrocortisone, cortols, cortolones, 11β-hydroxyaetiocholanolone, 11β-hydroxyandrosterone and 11-oxoaetiocholanolone in the fraction released by hydrolysis of the urinary steroid conjugates.
The excretion of 6β-hydroxycortisol in a group of patients with rheumatoid arthritis was not significantly greater than that in a similar group of normal subjects in whom the upper limit of the range was higher than values previously reported.
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SUMMARY
The major metabolic pathways of cortisol in a patient with sarcoidosis have been studied after intravenous injection of a tracer dose of [4-14C]cortisol. Results from some preliminary experiments in four other patients are also presented. The effects of large doses of cortisol on its metabolism were also studied.
In all the patients studied the adrenal secretion rate of cortisol was in the low normal range. The rate of disappearance of radioactivity from the plasma fractions containing the unconjugated steroids was normal before cortisol therapy but slower than normal during therapy. During therapy there was a significant decrease in the total urinary radioactivity.
In the one patient in whom detailed studies were made, an unusually large proportion of the urinary metabolites was in the unconjugated fraction in which the amount of 6β-hydroxycortisol was greater than normal. Apart from an increased ratio of 11β-hydroxy- to their corresponding 11-oxo-metabolites there was no essential difference in the pattern of excretion of the metabolites in this patient during therapy. In this patient only 65% of the injected radioactivity was excreted in urine after 48 hr., whereas the other patients excreted a normal percentage of the injected radioactivity during this period.
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ABSTRACT
Exposure of rainbow trout to a reduced ambient calcium level (from 490 to 25 μmol Ca2+/l) caused hypocalcaemia and induced a rapid increase (within 1 h) in systemic cortisol levels. Under conditions of low environmental calcium concentrations, cortisol levels remained increased for at least 8 days. After this time the in-vitro Ca2+-transport capacity of branchial basolateral membrane vesicles was increased due to stimulation of Ca2+-ATPase activity, presumably as a result of chloride cell proliferation. Pituitary prolactin cells were unaffected by low ambient calcium levels. Fish kept in water containing 490 μmol Ca2+/l and treated with cortisol for 7 days displayed an increase in whole body calcium uptake and an enhancement of the branchial calcium transport capacity; concomitantly, hypercalcaemia was observed. We conclude that, in the rainbow trout, cortisol exerts hypercalcaemic effects by stimulating Ca2+ uptake from the water and that this effect forms an intrinsic part of the established mineralocorticoid action of cortisol in fish.
Journal of Endocrinology (1989) 120, 75–82
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The effect of intracarotid perfusion of 40 mg cortisol for 1 h on the hormonal response to three different doses of an intramuscular injection of synthetic gonadotrophin releasing hormone (GnRH) was compared to that of GnRH injected during intracarotid perfusion with 0·9% (w/v) NaCl solution in five boars. The increase in production of LH, above basal values, in response to injection of 0·25 μg GnRH midway through perfusion was only slightly greater (P > 0·05) in boars receiving cortisol compared to that when the same boars received saline. When 0·5 μg GnRH was injected midway through perfusion, a significantly greater (P<0·05) increase in production of LH above basal levels occurred during cortisol administration than occurred when saline was given. Injection of 1·0 μg GnRH in boars during cortisol perfusion resulted in significantly greater (P<0·01) production of LH, above basal levels, compared to the increase above basal levels that resulted when this dose of GnRH was given during intracarotid saline treatment. Increases in plasma values of testosterone reflected the increases in levels of LH. The results suggest that acute elevations in plasma cortisol may, under some circumstances, enhance the increased production of LH in the boar by increasing the responsiveness of the anterior pituitary gland to GnRH.
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ABSTRACT
The effects of cortisol on hepatic and renal gluconeogenic enzyme activities were investigated in sheep fetuses during late gestation and after experimental manipulation of plasma cortisol levels by fetal adrenalectomy and exogenous infusion of cortisol. Hepatic and renal gluconeogenic enzyme activities increased with increasing gestational age in parallel with the normal rise in fetal cortisol levels towards term (146± 2 days). For the majority of enzymes this increase in activity towards term was prevented when the prepartum cortisol surge was abolished by fetal adrenalectomy and stimulated prematurely in fetuses younger than 130 days by exogenous infusion of cortisol. When the data from all the fetuses were combined irrespective of treatment or gestational age, there were significant positive correlations between the log plasma cortisol concentration in utero and the activities of glucose-6-phosphatase, fructose diphosphatase, phosphoenolpyruvate carboxykinase and aspartate transaminase in the fetal liver and kidney, and pyruvate carboxylase in the fetal liver but not in the kidney. No correlation was observed between log plasma cortisol and alanine aminotransferase activity in either fetal liver or kidney. These findings show that cortisol is a physiological regulator of most of the fetal gluconeogenic enzymes and enhances the glucogenic capacity of the sheep fetus during late gestation.
Journal of Endocrinology (1993) 137, 213–222
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ABSTRACT
We have observed previously that the rate of cortisol catabolism by lymphocytes (CCL) was indicative of the vulnerability of these cells to cortisol. We attempted to ascertain whether cortisol-sensitive lymphocytes (e.g. thymocytes) metabolize cortisol at a different rate from cortisol-resistant cells and whether lymphocytes in which cortisol catabolism is inhibited become cortisol sensitive. The work was facilitated by the observation that an ethanol extract plasma from patients with acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC) had the capacity to inhibit CCL.
The capacity of thymocytes to metabolize cortisol was found to be 11 times lower than that of peripheral lymphocytes. Inhibition of CCL with an ethanol extract of plasma from AIDS/ARC patients made the cells vulnerable to cortisol, causing them to die at a rate seven times greater than that of control samples. It is suggested that these findings may have important implications with regard to the nature of lymphocyte depletion in AIDS/ARC patients or in people at risk of developing the syndrome.
J. Endocr. (1987) 112, 259–264
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SUMMARY
The results of serial glucose tolerance tests in cortisol-treated, thyroidectomized calves indicate that there is a progressive reduction in the tolerance to glucose and that this is associated with a diminution in the rise in plasma insulin concentration which normally occurs in response to hyperglycaemia. These experimental conditions also stop growth within 12–14 days. All these effects are reversed by injections of thyroxine at a dose which raises the plasma thyroxine concentration to normal values for 7 days in spite of the continued administration of cortisol.
These results suggest that, in the unweaned thyroidectomized calf, daily injections of cortisol reduce the sensitivity of the insulin release mechanism, which may provide an explanation for the severe diabetic syndrome which is known to develop under these conditions.
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University of Oxford, Nuffield Institute for Medical Research, and John Radcliffe Hospital, Department of Obstetrics & Gynaecology, Headley Way, Headington, Oxford, 0X3 9DU
(Received 9 March 1976)
Setchell, Shackleton & Himsworth (1975) recently reported the effects of the sedative Sernylan (phencyclidine hydrochloride) on the concentration of cortisol in the plasma of non-pregnant rhesus monkeys. It was found that after an early decline, plasma cortisol increased gradually during a 4 - 5 h period of prolonged sedation. In our department, some non-pregnant monkeys are routinely bled without anaesthesia. These animals have been trained to jump from their cage into an aluminium box with an adjustable foam-lined lid, which allows them to be restrained gently during sampling from the saphenous vein. The present communication compares the plasma cortisol concentrations in monkeys that had become used to this sampling procedure over several months, with values measured in unanaesthetized animals that had not previously
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It has been suggested that in or on erythrocytes there is a substance capable of binding cortisol as strongly as transcortin but having a lower capacity than the latter (Sandberg, Slaunwhite & Carter, 1960; De Moor, Heirwegh, Heremans & Declerck-Raskin, 1962; De Moor & Steeno, 1962). Such a binding agent should compete with plasma transcortin and thus influence cortisol distribution between erythrocytes and plasma. Since the capacity of the hypothetical agent is said to be low (Sandberg et al. 1960), competition must be looked for at low cortisol levels. The authors have used corticoid-poor (12 p.m.) blood to study this aspect of corticoid distribution. With fluorimetric techniques a definite upswing of the erythrocyte uptake curve was noted at a mean plasma corticoid level of 7·1 μg./100 ml. (De Moor & Steeno, 1962). Since this could be due to differences in the specificity of both fluorimetric techniques, experiments with tritium-labelled steroids