| http://purl.uniprot.org/citations/14688446 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/14688446 | http://www.w3.org/2000/01/rdf-schema#comment | "It has been reported that the melanocortin 4-receptor (MC4-R) may act downstream of leptin to mediate its effects on food intake and several neuroendocrine functions (the reproductive system, the hypothalamo-pituitary-thyroid axis, and prolactin secretion). However, no previous study examined whether MC4-R mediates leptin stimulatory actions on growth hormone (GH) secretion, or whether MC4-R signaling is involved in spontaneous pulsatile GH release in fed rats. Therefore in this study we examined the involvement of both MC3-R and MC4-R (the predominant MC-R subtypes expressed in the brain) in these two aspects of GH secretion in freely-moving male rats. In both fed and 3-day fasted rats, plasma GH levels were determined every 15 min over 5 h after single intracerebroventricular injections of the following substances or vehicle. Fasting diminished and leptin (0.3 nmol) reinstated the GH pulse amplitude without affecting the pulse frequency. Neither HS014 (1.0 nmol, a selective MC4-R antagonist) nor agouti-related peptide (1.0 nmol, a non-selective MC3/4-R antagonist) was effective in altering leptin-stimulated or spontaneous GH secretion. In addition, neither melanotan-II (1.0 nmol, a non-selective MC3/4-R agonist) nor gamma(1)-melanocyte-stimulating hormone (10 nmol, a selective MC3-R agonist) affected significantly GH release in fasted rats. We have previously demonstrated that stimulation or blockade of MC4-R, achieved by the same drug dosage as in this study, significantly affect luteinizing hormone and prolactin secretion in rats. The present results thus suggest that neither MC4-R nor MC3-R is involved in leptin-stimulated or spontaneous GH secretion, or at least that the level of MC4-R involvement in GH secretion is much lower than that in luteinizing hormone and prolactin release regulation."xsd:string |
| http://purl.uniprot.org/citations/14688446 | http://purl.org/dc/terms/identifier | "doi:10.1159/000074886"xsd:string |
| http://purl.uniprot.org/citations/14688446 | http://purl.uniprot.org/core/author | "Yoneda M."xsd:string |
| http://purl.uniprot.org/citations/14688446 | http://purl.uniprot.org/core/author | "Watanobe H."xsd:string |
| http://purl.uniprot.org/citations/14688446 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
| http://purl.uniprot.org/citations/14688446 | http://purl.uniprot.org/core/name | "Neuroendocrinology"xsd:string |
| http://purl.uniprot.org/citations/14688446 | http://purl.uniprot.org/core/pages | "331-338"xsd:string |
| http://purl.uniprot.org/citations/14688446 | http://purl.uniprot.org/core/title | "Evaluation of the role of melanocortin 3 and 4 receptors in leptin-stimulated and spontaneous growth hormone secretion in rats."xsd:string |
| http://purl.uniprot.org/citations/14688446 | http://purl.uniprot.org/core/volume | "78"xsd:string |
| http://purl.uniprot.org/citations/14688446 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/14688446 |
| http://purl.uniprot.org/citations/14688446 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/14688446 |
| http://purl.uniprot.org/uniprot/#_P70596-mappedCitation-14688446 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/14688446 |
| http://purl.uniprot.org/uniprot/#_A6IXT4-mappedCitation-14688446 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/14688446 |
| http://purl.uniprot.org/uniprot/A6IXT4 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/14688446 |
| http://purl.uniprot.org/uniprot/P70596 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/14688446 |