Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute stresses such as trauma or endotoxemia augment GLN demand and are associated with increased release of this amino acid from skeletal muscle and lung as well as increased expression of glutamine synthetase (GS, the principal enzyme of GLN synthesis) in these tissues. Muscle GLN release is also increased during chronic catabolic states which are associated with depletion of lean body mass, such as starvation or malignancy. We hypothesized that the expression of GS in response to an acute stress would be altered in tumor-bearing rats (TBR) experiencing severe cachexia and therefore a previously heightened GLN demand. Male Fischer 344 rats were implanted with methylcholanthrene-induced fibrosarcoma tumors or underwent sham operations and pair-feeding (sham) with TBR partners. When tumor burden reached approximately 15% of carcass weight, animals received injections of either Escherichia coli lipopolysaccharide (LPS, 1 mg/kg body wt) or saline vehicle. Rats were sacrificed 8 h after injection and lung and muscle tissue were analyzed for GS mRNA and protein via Northern and Western blot techniques, respectively. LPS injection caused an equivalent 4- to 6-fold increase in lung and muscle GS mRNA in both TBR and sham rats (P < 0.01). LPS did not produce a significant increase in GS protein level in muscle tissue of either group or in lung tissue of sham rats. In contrast, endotoxin did lead to a 3.5-fold increase in GS protein levels in lung tissue of TBRs (P < 0.05). This increase in lung GS protein may signify the importance of the lung in maintaining GLN homeostasis during chronic catabolic states where muscle mass is diminished.
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PMID:Sepsis increases lung glutamine synthetase expression in the tumor-bearing host. 973 11

The ongoing hypermetabolic response in patients with prolonged critical illness leads to the loss of lean tissue mass. Since the cachexia of prolonged illness is usually associated with low concentrations of anabolic hormones, hormonal intervention has been thought to be beneficial. However, most interventions have been shown to be ineffective and their indiscriminate use even causes harm. Before considering endocrine intervention in these frail patients, a detailed understanding of the neuroendocrinology of the stress response is warranted. It is now clear that the acute phase and the later phase of critical illness behave differently from an endocrinological point of view. The acute stress response consists primarily of an actively-secreting pituitary in the presence of low circulating peripheral anabolic hormones, suggesting resistance of the peripheral tissues to the effects of anterior pituitary hormones. However, when the disease process becomes prolonged, there is a uniformly-reduced pulsatile secretion of anterior pituitary hormones with proportionally reduced concentrations of peripheral anabolic hormones. The origin of this suppressed pituitary secretion is located in the hypothalamus, as hypothalamic secretagogues can reactivate the anterior pituitary and restore pulsatile secretion. The reactivated pituitary secretion is accompanied by an increase in peripheral target hormones, indicating at least partial sensitivity of these tissues to anterior pituitary hormones in this chronic phase of illness. Thus, endocrine intervention with a combination of hypothalamic secretagogues that more completely reactivate the anterior pituitary could be a more physiological and effective strategy for inducing anabolism in patients with prolonged critical illness.
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PMID:Endocrine modifications and interventions during critical illness. 1537 56

During the prolonged phase of critical illness, the ongoing hypermetabolic response leads to loss of lean tissue mass. Although the cachexia of prolonged illness is usually associated with low concentrations of anabolic hormones, most endocrine interventions attempting to correct the hormone balance have shown to be ineffective and their indiscriminate use is even harmful. Thus, a detailed understanding of the neuroendocrinology of the stress response is warranted, especially as the acute and chronic phases show remarkable differences. In the acute stress response, low circulating peripheral anabolic hormone levels, despite an actively secreting pituitary, are indicative of peripheral resistance to the anterior pituitary hormones. By contrast, the pulsatile secretion of anterior pituitary hormones is uniformly decreased in the prolonged phase of the disease, leading to proportionally reduced concentrations of peripheral anabolic hormones. As hypothalamic secretagogues can restore the pulsatile secretion of the anterior pituitary and increase peripheral target hormones, tissues are at least partially sensitive to the anterior pituitary hormones in this phase of illness. Therefore, a combination of hypothalamic secretagogues that reactivates the anterior pituitary to a greater extent could be a more physiological and effective strategy to induce anabolism in patients with prolonged critical illness.
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PMID:Hormonal and metabolic strategies to attenuate catabolism in critically ill patients. 1552 54