Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alterations of glucose metabolism were investigated for 6 hours following an intraarterial injection of murine recombinant granulocyte-monocyte colony-stimulating factor (GM-CSF) (30 micrograms/kg body weight). GM-CSF resulted in a transient elevation of plasma glucose. The rate of whole body glucose appearance, as measured by infusion of [6-3H] glucose, was increased by about 10% between 0.5 and 3 hours following GM-CSF injection. In vivo glucose utilization of individual tissues was investigated by the tracer 2-deoxyglucose technique. At 30 min, GM-CSF increased glucose utilization by 80-90% in liver and lung, and 50-60% in skin and spleen. At 3 and 6 hours, glucose utilization by these tissues returned toward control levels except for lung. There was a 40-50% increase in glucose utilization by skeletal muscle 30 min after GM-CSF which was sustained for 6 hours. Glucose utilization of testis, ileum and kidney did not change significantly. Plasma concentrations of insulin, glucagon and tumor necrosis factor were not altered in response to GM-CSF. These findings indicate that some of the acute metabolic effects of a short-term administration of GM-CSF are observed in macrophage-rich tissues, and suggest that GM-CSF may be involved in the metabolic upregulation of immunologically active tissues.
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PMID:Upregulation of glucose metabolism by granulocyte-monocyte colony-stimulating factor. 187 98

In 19 normal subjects an increase in the number of circulating neutrophils was observed after intramuscular injection of 1 mg glucagon. The response began at the end of the 1st hour following the injection and persisted beyond the 8th hour, with a peak between 2 and 5 hours. No response was obtained in patients with bone marrow aplasia, either primary or associated with acute leukaemia. In 20 patients with chronic primary neutropenia, the degree of response was proportional to the percentage of medullary polymorphonuclears. A comparison between the kinetics of the glucagon-induced granulocyte response and that of the response induced by other neutrophil mobilizing agents suggested that glucagon acts by releasing granulocytes from the bone marrow reserve compartment. The finding that an infusion of dibutyryl cyclic AMP results in granulocyte mobilization suggests that the effects of glucagon are mediated by cAMP at cell level. Since the glucagon response test is harmless and gives rapid and pronounced results, it may be useful in investigation of patients with neutropenia. In addition, the glucagon-induced granulocyte mobilization might improve leucocyte yield in blood donors used for transfusion in agranulocytosis.
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PMID:[Glucagon-induced neutrophil mobilization (author's transl)]. 707 58

Superoxide anion (O2-) production and bactericidal capacity of morphologically mature bone marrow polymorphonuclear neutrophils (PMN) were evaluated in 30 haematologically normal individuals. These same parameters of peripheral PMNs were estimated in 15 healthy volunteers before and after glucagon-induced marrow granulocyte reserve mobilization. Bone marrow PMN in comparison with cells obtained from peripheral blood manifested impaired superoxide anion production and diminished bactericidal capacity. The admixture of bone marrow PMN released into the circulation by the use of glucagon administration significantly lowered both estimated PMN functions.
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PMID:Superoxide anion (O2-) production and bactericidal capacity of polymorphonuclear neutrophils obtained from patients subjected to glucagon test. 896 52

Chemotherapy agents induce apoptotic cell death and loss of cell proliferation in the intestinal crypt epithelium, resulting in intestinal mucosal damage called "mucositis". Small intestinal mucositis is characterized structurally by crypt loss and villus atrophy, and functionally by absorptive and barrier impairments. The increased use of chemotherapy in cancer treatment and the clinical importance of the intestinal mucositis as a common side effect have stimulated more active research into understanding the pathophysiology of intestinal mucositis and developing agents for preventing or treating this condition. Rodent studies have shown that, following the chemotherapy-induced initial apoptosis and loss of crypt cell proliferation, many different growth factors or their receptors are upregulated locally at the crypts, preceding or coinciding with the epithelial hyperproliferative repair response. Aiming to reduce crypt cell apoptotic sensitivity to cytotoxic chemotherapy and/or to enhance crypt epithelial proliferative repair, several exogenous growth factor treatments have been tested, either preclinically and/or clinically, and are showing promise for their efficacy or safety in preventing or treating chemotherapy-induced mucositis. These tested growth factors include keratinocyte growth factor, interleukin-11, transforming growth factor beta, milk-derived growth factor extract, macrophage/granulocyte colony stimulating factors, and glucagon-like peptide 2. Further research on the basic and discovery levels and subsequent translational studies are needed to understand more about chemotherapy-induced intestinal mucositis and to identify candidates of growth factors or other agents that will potentially prevent or treat chemotherapy-induced mucositis more effectively, specifically, safely, and practically in chemotherapy patients.
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PMID:Roles of growth factors in chemotherapy-induced intestinal mucosal damage repair. 1452 28