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Endotoxin administration increases hypothalamic somatostatin mRNA through nitric oxide release

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dc.contributor.author Priego, Teresa
dc.contributor.author Ibáñez de Cáceres, Inmaculada
dc.contributor.author Martín Velasco, Ana Isabel
dc.contributor.author Villanúa, María de los Ángeles
dc.contributor.author López-Calderón, Asunción
dc.date.accessioned 2016-08-01T08:47:47Z
dc.date.available 2016-08-01T08:47:47Z
dc.date.issued 2005
dc.identifier.citation Priego, T., Ibáñez de Cáceres, I., Martín, A. I., Villanúa, M. A., & López-Calderón, A. (2005). Endotoxin administration increases hypothalamic somatostatin mRNA through nitric oxide reléase. Regulatory Peptides, 124(1-3), 113-118. spa
dc.identifier.issn 01670115
dc.identifier.uri http://hdl.handle.net/11268/5528
dc.description.abstract Acute inflammation induced by endotoxin (LPS) administration inhibits insulin-like growth factor (IGF-I) and growth hormone (GH) secretion. The aim of this study was to elucidate the role of glucocorticoids and nitric oxide (NO) in the effect of LPS on hypothalamic somatostatin gene expression. Adult male Wistar rats were injected with different doses of LPS (5, 10 and 100 μg/kg). Rats received two i.p. injections of LPS (at 17:30 and 8:30 h the following day) and were killed 4 h after the second injection. LPS administration at the dose of 100 μg/kg increased the hypothalamic somatostatin mRNA content, as well as the serum concentrations of corticosterone. Glucocorticoids do not seem to be involved in LPS-induced increase in hypothalamic somatostatin mRNA since adrenalectomy did not prevent this effect. In order to analyze the possible effect of NO, aminoguanidine, an inducible nitric oxide synthase inhibitor, was injected (100 mg/kg s.c.) simultaneously with LPS injection. Aminoguanidine administration did not modify somatostatin mRNA in saline injected rats, but it prevented LPS-induced increase in hypothalamic somatostatin mRNA. These data suggest that the stimulatory effect of endotoxin on hypothalamic somatostatin gene expression is not mediated by glucocorticoids, but instead by the increase in NO release. spa
dc.description.sponsorship SIN FINANCIACIÓN spa
dc.language.iso eng spa
dc.title Endotoxin administration increases hypothalamic somatostatin mRNA through nitric oxide release spa
dc.type article spa
dc.description.impact 2.272 JCR (2005) Q2, 34/75 Physiology; Q3, 46/89 Endocrinology & metabolism spa
dc.identifier.doi 10.1016/j.regpep.2004.07.001
dc.rights.accessRights closedAccess spa
dc.subject.uem Fisiología humana spa
dc.subject.uem Farmacología clínica spa
dc.subject.unesco Fisiología humana spa
dc.subject.unesco Farmacología spa
dc.description.filiation UEM spa
dc.peerreviewed Si spa


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