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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Resting oxygen consumption was elevated by 30% in young rats fed a cafeteria diet compared with their chow-fed controls and by 22% in cafeteria-fed, adrenalectomized (ADX) rats compared with the ADX chow-fed group, but injection of propranolol reduced oxygen consumption in the cafeteria-fed animals and abolished these differences. Brown adipose tissue (BAT) mass was increased by cafeteria feeding, and the activity of the mitochondrial proton conductance pathway (assessed from purine nucleotide binding) was enhanced by adrenalectomy and by cafeteria feeding. Norepinephrine turnover in BAT (determined from the time-dependent loss of tissue [3H]norepinephrine specific activity) was increased by 105% in sham-operated, cafeteria-fed rats, by 142% in chow-fed ADX rats, and by 400% in cafeteria-fed ADX rats, compared with chow-fed controls. Cardiac norepinephrine turnover was elevated by 80% in sham-operated, cafeteria-fed rats, but unaffected by adrenalectomy. These data indicate that the enhanced thermogenesis and BAT activity induced by adrenalectomy in chow- or cafeteria-fed rats is due to increased sympathetic activity in the tissue.
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PMID:Thermogenesis and sympathetic activity in BAT of overfed rats after adrenalectomy. 345 37

Female obese and lean Zucker rats were adrenalectomized (ADX) or sham-operated at 4 wk of age. ADX animals were given daily injections of 0.01, 0.05, 0.50, 1.0, or 2.0 mg hydrocortisone/100 g body wt for 30 days. ADX rats gained less weight than sham-operated controls. Obese ADX rats at the lowest dose (0.01) had a net positive energy gain but lost body fat. As steroid dose increased, obese rats deposited more fat and less protein. Doses of 0.01 and 0.05 mg produced rats that were less fat than sham-operated controls, whereas doses of 0.50, 1.0, and 2.0 mg produced rats of comparable body fat composition. Obese rats were consistently fatter and had a significantly smaller percentage body protein than lean rats at each dose. Body fat elevation was reflected by heavier parametrial and retroperitoneal fat depots and larger fat cells at all doses except the lowest. Compared with sham-operated controls, lean and obese rats at the two lowest replacement doses (0.01, 0.05) exhibited significantly decreased plasma insulin and triglyceride levels and significantly elevated brown adipose tissue protein content and citrate synthase (CS) activity. Obese rats at these doses had significantly reduced adipose tissue lipoprotein lipase (LPL) activity in the retroperitoneal depot and lower food intake. Furthermore, these obese rats had adipose depot weights, cell sizes, LPL activity, and plasma insulin, glucose, and triglyceride comparable to that of lean sham-operated controls. As steroid dose increased (0.5, 1.0, 2.0), plasma insulin and triglyceride and food intake markedly increased only in obese rats. Adipose tissue LPL activity appeared unaffected by dose. Brown adipose tissue protein content and CS activity significantly decreased as dose increased in both lean and obese rats. At all doses of replacement obese rats were more responsive to steroid than were lean rats. Obese rats receiving 0.01 mg had comparable fat depot weights, cell sizes, and plasma insulin and triglyceride as lean rats receiving 50 times as much steroid per day (0.50 mg). These results suggest glucocorticoids play an important role in the early development of obesity in the Zucker rat and support the hypothesis that obese rats are more responsive to glucocorticoids than are lean rats.
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PMID:Effect of adrenalectomy and glucocorticoid replacement on development of obesity. 351 71

Successful induction of the experimental autoimmune disease allergic encephalomyelitis (EAE) depends, in part, upon species susceptibility. The Lewis rat is highly susceptible to EAE whereas the Brown Norway (BN) strain is resistant to induction. Endogenous glucocorticoids influence the manifestation of the disease and recovery from neurological deficits. Moreover, abrogation of the curative steroid-mediated effects converts the condition to a terminal state. In the present study treatment of EAE-inoculated BN rats with the steroid antagonist RU486 (Mifepristone) failed to influence the resistance to symptoms. Similarly, adrenalectomy (ADX) prior to sensitisation did not allow the development of clinical EAE but did facilitate neuroperivascular accumulation of inflammatory-type cells. However, RU486 treatment after ADX induced neurological and histological signs of EAE in the majority of animals. Lymphocyte proliferation studies on cells isolated from BN rats treated with RU486 revealed an enhanced responsiveness to mitogenic and antigenic stimulation. These results strongly implicate endogenous steroids in the expansion of immune cell numbers which would be an absolute requirement for the expression of autoimmune-based neurological disease in otherwise resistant rats.
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PMID:Endogenous corticosteroids modulate lymphoproliferation and susceptibility to experimental allergic encephalomyelitis in the Brown Norway rat. 781 61

This study was designed to examine adrenocortical function in old (30 months) and young (6 months) male Brown Norway rats. The following observations were made. First, stress induced a higher pituitary adrenocorticotropic hormone (ACTH) response in the aged male Brown Norway rats than in young rats, while peak circulating corticosterone (CORT) levels were not different. Moreover, this type of "repeated" stress involving subcutaneous injection and blood sampling at various time points by pinching the tail vein, evoked a prolonged ACTH and CORT response in the aged animal. Second, exogenous ACTH1-24 administered to dexamethasone-pretreated Brown Norway rats, used as an in vivo challenge test for adrenocortical function, resulted in a delayed CORT response in the aged rats. The termination of the CORT response to ACTH, however, was not different between young and old rats. Third, ACTH1-24 stimulation of adrenocortical cells in vitro showed a tendency to a reduced CORT output, when these cells were obtained from old animals. Fourth, adrenalectomy (ADX) differentially affected pituitary ACTH release at both ages. The initial post-ADX ACTH surge was more pronounced in the aged animals. Beyond 4 days post-ADX the old Brown Norway rats did not show the pronounced afternoon peak in circulating ACTH as was observed in the young animals. This study demonstrates that during the aging process a deficiency in adrenocortical function develops in the male Brown Norway rat. This deficiency involves a less efficient stress-induced activation of adrenocortical output of CORT having enhanced pituitary ACTH release as one of the consequences.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adrenocortical hyporesponsiveness and glucocorticoid feedback resistance in old male brown Norway rats. 787 84

During the dark phase of the diurnal cycle, and during recovery from restraint stress, Brown Norway (BN) rats secrete less corticosterone than Fischer 344 (F344) rats. These strains also display different levels of corticosteroid receptors in the hippocampus, and of plasma transcortin. Because corticosteroid receptors, plasma transcortin and corticosterone secretion are mutually regulated, we examined brain and pituitary mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) expression and some of the parameters modulated by these receptors (i.e. body and thymus weight, fluid intake, plasma transcortin) in BN and F344 rat strains, by comparing the effects of either hormone deprivation by long-term (21 days) adrenalectomy (ADX), or chronic elevation of corticosterone given in drinking fluid to ADX rats. In BN rats, body weight gain and fluid intake were insensitive to corticosterone deprivation, suggesting that MR-related mechanisms are constitutively active in this strain. Body weight (b.w.) gain, plasma transcortin and thymus weight were reduced to a greater extent by chronic corticosterone in BN rats than in F344 rats, possibly as a consequence of higher free, active fraction of plasma corticosterone due to lower plasma transcortin concentrations and/or a greater efficiency of GR-related mechanisms in BN rats. F344 rats displayed twofold higher brain and pituitary MR levels than BN rats, whereas tissue-and strain-specific regulations were observed for GR levels. The differences in MR levels observed between BN and F344 strains cannot completely explain the differences in corticosterone actions, suggesting that strain differences in response to ADX or corticosterone treatment result from variable receptor efficiencies.
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PMID:Strain differences in corticosteroid receptor efficiencies and regulation in Brown Norway and Fischer 344 rats. 1022 80

In a previous study using corticosterone treatment of adrenalectomized rats, we hypothesized that mineralocorticoid receptor (MR)-related mechanisms are constitutively active and that glucocorticoid receptor (GR)-mediated mechanisms are more efficient in Brown Norway rats compared to Fischer 344 (F344) rats. In order to discriminate the mineralocorticoid from the glucocorticoid actions exerted by corticosterone, F344 and Brown Norway adrenalectomized rats were treated with increasing doses (1, 5 and 25 microg/ml of drinking water) of deoxycorticosterone (DOC, MR-specific ligand) or RU 28362 (GR-specific ligand). These rats were compared with long-term adrenalectomized (ADX) untreated rats and sham-ADX rats. This study confirms our previous results, notably the lack of effect of ADX on body weight and fluid intake in Brown Norway rats. Moreover, DOC treatment had no effect in Brown Norway rats whereas the higher dose restored fluid intake of the F344 ADX group to sham values. These results support the hypothesis of a constitutive activation of the MR and therefore the insensitivity of this receptor to its ligand in Brown Norway rats. Alternatively, RU 28362 treatment induced greater weight loss, decrease in food intake, anxiolysis, thymus involution, and decrease in plasma transcortin concentration and pituitary corticosteroid receptor densities in Brown Norway rats than in F344 rats, which is consistent with greater efficiency of GR mechanisms in Brown Norway rats than in F344 rats. Therefore, these strains are of great utility to disentangle MR and GR effects on complex phenotypes.
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PMID:Is the mineralocorticoid receptor in Brown Norway rats constitutively active? 1084 87

Our previous studies suggested that the mineralocorticoid receptor (MR) of Brown Norway (BN) male rats is active independently of the presence of its ligands (i.e. constitutively active), and that glucocorticoid receptor (GR)-mediated mechanisms are more efficient in BN than in Fischer 344 (F344) male rats. Such functional differences in corticosteroid receptors led us to compare the effect of adrenalectomy (ADX) and MR/GR-mediated actions (treatments with deoxycorticosterone, DOC and RU 28362, respectively) on female rats from both strains, and, within the framework of a genetic study, to investigate how these differences were inherited in rats of the first generation (F1) born from the crossbreeding between BN and F344 inbred rats. This study extends our previous hypotheses of a constitutive activation of MR and of a greater efficiency of GR in males to females of the BN strain. In both strains, female rats were less sensitive to ADX and to treatments with DOC or RU 28362 than males. Globally, F1 hybrid BNxF344 rats inherited the functional characteristics of MR and GR of BN rats.
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PMID:Effects of adrenalectomy and of mineralocorticoid receptor/glucocorticoid receptor ligands in female Brown Norway and Fischer 344 rats and f1 hybrids. 1212 95

Our previous studies showed that adrenalectomy (ADX) has surprisingly no effect on body weight and fluid intake in the Brown Norway rat strain, suggesting that mineralocorticoid receptor (MR)-mediated effects are present even in absence of corticosteroids in this strain. Moreover, glucocorticoid receptor (GR)-mediated mechanisms are more effective in Brown Norway than in Fischer 344 rats. Such functional differences in corticosteroid receptor pathways between Brown Norway and Fischer 344 rats led us to compare the effect of ADX and MR/GR-mediated actions on sodium and potassium excretion between these two rat strains. To this end, we first measured the effect of an acute high dose of aldosterone on the urinary Na+/K+ concentration ratio in intact and ADX Brown Norway and Fischer 344 rats. Second, to discriminate mineralocorticoid from glucocorticoid actions, we treated chronically ADX rats with increasing doses of aldosterone or RU28362, a pure GR agonist, in the drinking fluid. As sodium homeostasis involves salt appetite regulation, behaviour under mineralocorticoid control, we also measured saline preference in Brown Norway and Fischer 344 rats. Our data illustrate: (1) the very limited effect of ADX on body weight, food and fluid intake, diuresis, natriuresis, kaliuresis and salt appetite in Brown Norway rats, supporting the presence of MR signalling pathways in the absence of adrenal steroids in these rats; (2) the insensitivity of MR to aldosterone in intact Brown Norway rats, and the reduced sensitivity of MR to aldosterone in ADX Brown Norway rats compared with ADX Fischer 344 rats; and (3) the greater sensitivity of GR-related mechanisms to RU28362 in Brown Norway than in Fischer 344 rats in terms of body weight gain and electrolyte excretion. Considering that both MRs and GRs regulate hypothalamic-pituitary-adrenal axis processes, such functional differences in corticosteroid receptors could be at the origin, at least partly, of the strain differences in corticotropic activity/reactivity to stress previously described.
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PMID:Excretion of electrolytes in Brown Norway and Fischer 344 rats: effects of adrenalectomy and of mineralocorticoid and glucocorticoid receptor ligands. 1536 79

Trichomonas vaginalis has been reported to possess alternative 2-keto acid oxidoreductases (KORs). These enzymes preferentially used indolepyruvate in a reaction that resembled that of pyruvate:ferredoxin oxidoreductase (PFO). However, the KORs did not reduce ferredoxin and remained active in metronidazole-resistant trichomonads lacking PFO. Therefore, it was proposed that the KORs may help trichomonads to survive in the presence of metronidazole. The KORs were identified using activity staining on native gels (Brown DM, Upcroft JA, Dodd HN, et al. Alternative 2-keto acid oxidoreductase activities in T. vaginalis. Mol Biochem Parasitol 1999;98:203-14). In the current study, we showed that the apparent KOR activity was caused by the non-enzymatic reduction of the indicator dye, nitroblue tetrazolium, by indolepyruvate, which is facilitated by Triton X-100 used to prepare the membrane fractions. We could not confirm the presence of KORs in metronidazole-resistant T. vaginalis. The low level indolepyruvate-dependent activity that is present in T. vaginalis strains sensitive to metronidazole is catalyzed by PFO, which was verified using the pure enzyme. Therefore, our results suggest that alternative 2-keto acid oxidoreductases do not exist in T. vaginalis.
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PMID:Alternative 2-keto acid oxidoreductases in Trichomonas vaginalis: artifact of histochemical staining. 2196 39