Cortisol and Corticotrophin in Burned Patients

Vaughan, George M.; Becker, Richard A.; Allen, John P.; Goodwin, Cleon W.; Pruitt, Basil A.; Mason, Arthur D.

doi:10.1097/00005373-198204000-00001

Cited by 157 publications

(56 citation statements)

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“…As a result, roughly 30% of all patients diagnosed with cancer ultimately die of cachexia, underscoring the clinical relevance of this disorder [35][36][37][38]. In addition to the Metabolic Syndrome and cancer cachexia, dysfunctional GC action has been described in septic patients A c c e p t e d M a n u s c r i p t 6 [39,40], thereby, broadening the spectrum of metabolic complications associated with aberrant GC levels.…”

Section: Conditions Of Elevated Gc Levelsmentioning

confidence: 99%

Glucocorticoids, metabolism and metabolic diseases

Vegiopoulos

Herzig

2007

Molecular and Cellular Endocrinology

440

370

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Since the discovery of the beneficial effects of adrenocortical extracts for treating adrenal insufficiency more than 80 years ago, glucocorticoids (GC) and their cognate, intracellular receptor, the glucocorticoid receptor (GR) have been characterized as critical components of the delicate hormonal control system that determines energy homeostasis in mammals.Whereas physiological levels of GCs are required for proper metabolic control, excessive GC action has been tied to a variety of pandemic metabolic diseases, such as type II diabetes and obesity. Highlighted by its importance for human health, the investigation of molecular mechanisms of GC/GR action has become a major focus in biomedical research. In particular, the understanding of tissue-specific functions of the GC-GR pathway has been proven to be of substantial value for the identification of novel therapeutic options in the treatment of severe metabolic disorders. Therefore, this review focuses on the role of the GC-GR axis for metabolic homeostasis and dysregulation, emphasizing tissue-specific functions of GCs in the control of energy metabolism.

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Section: Conditions Of Elevated Gc Levelsmentioning

confidence: 99%

Glucocorticoids, metabolism and metabolic diseases

Vegiopoulos

Herzig

2007

Molecular and Cellular Endocrinology

440

370

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“…Plasma levels of glucocorticoids are elevated both in patients (16) and experimental animals with sepsis (17). Administration of cortisol in humans (18) or corticosterone or dexamethasone in rats (19,20) resulted in increased muscle protein breakdown.…”

Section: Introductionmentioning

confidence: 99%

Energy-ubiquitin-dependent muscle proteolysis during sepsis in rats is regulated by glucocorticoids.

Tiao

Fagan²,

Roegner³

et al. 1996

J. Clin. Invest.

224

198

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Recent studies suggest that sepsis-induced increase in muscle proteolysis mainly reflects energy-ubiquitin-dependent protein breakdown. We tested the hypothesis that glucocorticoids activate the energy-ubiquitin-dependent proteolytic pathway in skeletal muscle during sepsis. Rats underwent induction of sepsis by cecal ligation and puncture or were sham-operated and muscle protein breakdown rates were measured 16 h later. The glucocorticoid receptor antagonist RU 38486 or vehicle was administered to groups of septic and sham-operated rats. In other experiments, dexamethasone (2.5 or 10 mg/kg) was injected subcutaneously in normal rats. Total and myofibrillar proteolysis was determined in incubated extensor digitorum longus muscles as release of tyrosine and 3-methylhistidine, respectively. Energydependent proteolysis was determined in incubated muscles depleted of energy with 2-deoxyglucose and 2,4-dinitrophenol. Levels of muscle ubiquitin mRNA and free and conjugated ubiquitin were determined by Northern and Western blot, respectively. RU 38486 inhibited the sepsis-induced increase in total and myofibrillar energy-dependent protein breakdown rates and blunted the increase in ubiquitin mRNA levels and free ubiquitin. Some, but not all, sepsisinduced changes in ubiquitin protein conjugates were inhibited by RU 38486. Injection of dexamethasone in normal rats increased energy-dependent proteolysis and ubiquitin mRNA levels. The results suggest that glucocorticoids regulate the energy-ubiquitin-dependent proteolytic pathway in skeletal muscle during sepsis.

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“…20]. In addition, they are known to be elevated after stresses such as alcohol exposure and traumatic injury, especially burns [21][22][23]. Given a body of literature that suggests that glucocorticoids serve to direct and maintain proper immune function under both normal circumstances [for review see ref .…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoids protect against suppression of T cell responses in a murine model of acute ethanol exposure and thermal injury by regulating IL-6

Faunce

Gregory

Kovacs

1998

Journal of Leukocyte Biology

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Previous reports by this laboratory demonstrated that acute alcohol exposure combined with a 15% body surface area dorsal scald injury results in significant reductions in delayed-type hypersensitivity (DTH) and splenocyte proliferative responses compared to either insult alone. Previous studies by this lab have also shown that these defects are mediated, in part, by increased production of interleukin-6 (IL-6). Because both alcohol exposure and thermal injury are known to modulate glucocorticoid (CORT) levels, and CORT regulates IL-6 gene expression, the relationship between circulating CORT and IL-6 production in burn ؉ ethanol mice was examined . At 24 and 48 h post-burn, a positive correlation existed between circulating CORT levels and measurements of cellular immune function. Administration of exogenous CORT to burn ؉ ethanol-treated mice resulted in significant restoration (to 60% of control) of DTH and splenocyte proliferative responses. This restoration was concomitant with a down-regulation of circulating and macrophage-derived IL-6. The specificity of CORT in modulating these responses was tested by assessing cellular immune function and IL-6 levels after glucocorticoid receptor blockade with RU486. Taken together, these data strongly suggest that under normal circumstances CORT protects burned mice from severe immune dysfunction, a protection that is not afforded to burn ؉ ethanol-treated mice. Furthermore, the immune dysfunction observed in burn ؉ ethanol mice may be due to a lack of glucocorticoid attenuation of IL-6. J. Leukoc. Biol. 64: 724-732; 1998.

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Cortisol and Corticotrophin in Burned Patients

Cited by 157 publications

References 0 publications

Glucocorticoids, metabolism and metabolic diseases

Glucocorticoids, metabolism and metabolic diseases

Energy-ubiquitin-dependent muscle proteolysis during sepsis in rats is regulated by glucocorticoids.

Glucocorticoids protect against suppression of T cell responses in a murine model of acute ethanol exposure and thermal injury by regulating IL-6

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