Radioimmunoassay (RIA) of Serum Corticosterone in Rat

Gwosdow-Cohen, A.; Chen, C. L.; Besch, E. L.

doi:10.3181/00379727-170-41391

Cited by 96 publications

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“…Adequate placement of the cannulae was tested with the drinking response to an ICV injection of angiotensin (25 ng in 5 ul phosphate-buffered saline; Novabiochem, Laiifelfingen, Switzerland) (21). The corticosteronemia of adrenalectomized rats was below the limit of detection of the radioimmunoassay (22). After a 10-day recovery period, fed intact or adrenalectomized rats were intracerebroventricularly injected with a bolus of leptin (3 ug per rat) given within 2 min in 3 ul.…”

Section: Methodsmentioning

confidence: 99%

Glucocorticoids as Counterregulatory Hormones of Leptin: Toward an Understanding of Leptin Resistance

et al. 1997

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The product of the ob gene, leptin, is a hormone secreted by adipose tissue that acts in the hypothalamus to regulate the size of the body fat depot. Its central administration has been shown to decrease food intake and body weight, while favoring energy dissipation. As glucocorticoids are known to play a permissive role in the establishment and maintenance of obesity syndromes in rodents, it was hypothesized that they do so by restraining the effect of leptin. Leptin injected intracerebroventricularly as a bolus of 3 ug in normal rats induced modest reductions in body weight and food intake. In marked contrast, the same dose of leptin had very potent and long-lasting effects in decreasing both body weight and food intake when administered to adrenalectomized rats. Further, glucocorticoid supplementation of adrenalectomized rats dose-dependently inhibited these potent effects of leptin. These data suggest that glucocorticoids play a key inhibitory role in the action of leptin. Under normal conditions, this inhibitory influence of glucocorticoids may prevent lasting hypophagia. In obesity with degrees of hypercorticism, it may contribute to "leptin resistance," whose etiology is still little understood. Diabetes 46:717-719, 1997 P revious experiments have shown that the pathology of rodents with obesity of genetic (1^4), dietary (5), or hypothalamic (6-8) origin can be normalized by adrenalectomy and restored by glucocorticoid replacement (1,7,8). More recently and specifically, it was observed that neuropeptide Y (NPY)-induced obesity-like defects were prevented by adrenalectomy (9). As leptin and NPY have, in normal rats, opposite effects on body weight and food intake (10-19) and as the presence of glucocorticoids favors intracerebroventricular (ICV) NPY-elicited effects (9), it was hypothesized that glucocorticoids could have an inhibitory effect on the action of leptin. This could partly explain why the effect of central or peripheral leptin in decreasing food intake or body weight gain, although definitively present, is relatively weak in amplitude in normal From the Laboratoires de Recherches Metaboliques, Geneva University Medical School, Geneva, Switzerland.Address correspondence and reprint requests to Dr. Katherine E. Zakrzewska, Laboratoires de Recherches Metaboliques, Geneva University Medical School, 64 avenue de la Roseraie, 1211 Geneva 4, Switzerland. E-mail: touabi@cmu.unige.ch.Received for publication 2 December 1996 and accepted in revised form 29 January 1997.ICV, intracerebroventricular; NPY, neuropeptide Y.rodents (11-13). Thus, the purpose of this study was to compare the effects of ICV leptin administration on body weight and food intake in normal and adrenalectomized rats. RESEARCH DESIGN AND METHODSIntact adult sham-operated female Sprague-Dawley rats (body weight, 285 ± 8 g; n = 5) and bilaterally adrenalectomized ones (body weight, 275 ± 5 g; n = 8) purchased from IFFA CREDO (L'Arbresle, France) were used. They were fed ad libitum a standard laboratory diet (Provimi-Lacta, Cossonay, Sw...

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Section: Methodsmentioning

confidence: 99%

Glucocorticoids as Counterregulatory Hormones of Leptin: Toward an Understanding of Leptin Resistance

et al. 1997

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“…The interassay coefficient of variation was 10 % and the intra-assay coefficient of variation was 6.5 %. Plasma corticosterone was measured using the method of Gwosdow-Cohen et al (1982). Plasma glucose was measured by the automated method of Trinder (1969).…”

Section: Plasma Hormones and Glucosementioning

confidence: 99%

Acute effects of corticosterone on tissue protein synthesis and insulin-sensitivity in rats in vivo

Southorn¹,

Palmer²,

Garlick³

1990

Biochemical Journal

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The effect of corticosterone treatment on the sensitivity of muscle protein synthesis to insulin infusion was assessed in postabsorptive young rats. To select the optimal time period for corticosterone treatment, protein synthesis was measured by injection of L-[2,6-3H]phenylalanine (1.5 mmol/kg body weight) 1, 4, 12 or 24 h after injection of corticosterone (5 mg/kg body wt.). Muscle protein synthesis was significantly decreased at 4 h and the effect was maximal by 12 h; liver protein synthesis was elevated at 12 h and 24 h. The dose-response of muscle protein synthesis to a 30 min infusion with 0-150 munits of insulin/h was then compared in rats pretreated with corticosterone (10 mg/100 g body wt.) or vehicle alone. When no insulin was infused, corticosterone inhibited protein synthesis in gastrocnemius muscle. High doses of insulin stimulated protein synthesis, but the inhibition by corticosterone was similar to that in the absence of insulin. At intermediate doses of insulin there was an increased requirement for insulin to elicit an equivalent response in muscle protein synthesis. Plantaris muscle responded in a manner similar to that of gastrocnemius, but neither soleus muscle nor liver responded significantly to insulin. These data suggest that corticosterone has two modes of action; one which is independent from and opposite to that of insulin, and a second which causes insulin-resistance through a decrease in sensitivity rather than a change in responsiveness.

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“…Plasma corticosterone was determined by radioimmunoassay as previously described with corticosterone antibody from Dr. G. Niswender of Colorado State University [15]. ACTH was assayed using a radioimmunoassay kit from Nichols Institute (San Juan Capistrano, Calif., USA) which measures only intact ACTH.…”

Section: Assay Of Acth and Corticosteronementioning

confidence: 99%

Effects of the IL-1 Receptor Antagonist on the IL-1- and Endotoxin-Induced Activation of the HPA Axis and Cerebral Biogenic Amines in Mice

Dunn¹

1999

Neuroimmunomodulation

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Endotoxin (lipopolysaccharide, LPS) and interleukin-1 (IL-1) are known to activate the hypothalamo-pituitary- adrenocortical (HPA) axis, as well as brain norepinephrine (NE) and indoleamine metabolism. Because LPS administration is known to induce the synthesis and secretion of IL-1, it has been proposed that IL-1 is the endogenous mediator of the response to LPS. This proposal has been tested using various antagonists of IL-1 with varied results. Therefore we have re-examined this question using a wide range of doses of the interleukin-1- receptor antagonist protein (IL-1ra) at various times after intraperitoneal LPS. The results indicate that IL-1ra at doses more than adequate to prevent responses to exogenously administered IL-1β, failed to significantly attenuate the increases in plasma ACTH and corticosterone and the cerebral catecholamine and indoleamine responses induced by intraperitoneal LPS in mice. IL-1ra was also ineffective when plasma ACTH and corticosterone were measured at longer times after LPS, although some trends towards attenuations were occasionally observed at 4 or 6 h. The latter is consistent with the time course of IL-1 induction by LPS. Intracerebroventricular administration of IL-1ra attenuated the endocrine and neurochemical responses to intraperitoneal IL-1β. However, intracerebroventricular IL-1ra failed to antagonize the HPA and neurochemical responses to intraperitoneal administration of LPS or to intravenous IL-1β. In all of these experiments, there were very close parallels between the HPA and the neurochemical responses, especially that of NE. We conclude that IL-1 does not mediate the HPA or the neurochemical responses to intraperitoneal LPS, although it may contribute in a minor way to the late HPA responses. However, IL-1 within the CNS may contribute to the responses to intraperitoneal IL-1, but not to intraperitoneal LPS or intravenous IL-1.

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Radioimmunoassay (RIA) of Serum Corticosterone in Rat

Cited by 96 publications

References 0 publications

Glucocorticoids as Counterregulatory Hormones of Leptin: Toward an Understanding of Leptin Resistance

Glucocorticoids as Counterregulatory Hormones of Leptin: Toward an Understanding of Leptin Resistance

Acute effects of corticosterone on tissue protein synthesis and insulin-sensitivity in rats in vivo

Effects of the IL-1 Receptor Antagonist on the IL-1- and Endotoxin-Induced Activation of the HPA Axis and Cerebral Biogenic Amines in Mice

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