Linked Life Data

17272395

Source:http://linkedlifedata.com/resource/pubmed/id/17272395

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-4-20
pubmed:abstractText
Neuropeptide Y, a neuropeptide abundantly expressed in the brain, has been implicated in the regulation of the hypothalamo-pituitary-somatotropic axis and the hypothalamo-pituitary-gonadotropic axis. Elevated hypothalamic neuropeptide Y expression, such as that occurs during fasting, is known to inhibit both of these axes. However, it is not known which Y receptor(s) mediate these effects. Here we demonstrate, using Y receptor knockout mice, that Y2 and Y4 receptors are separately involved in the regulation of these axes. Fasting-induced inhibition of hypothalamic GHRH mRNA expression and reduction of circulating IGF-I levels were observed in wild-type and Y4(-/-) mice but not Y2(-/-) or Y2(-/-)Y4(-/-) mice. In contrast, fasting-induced reduction of GnRH expression in the medial preoptic area and testis testosterone content were abolished in the absence of Y4 receptors. Colocalization of Y2 receptors and GHRH in the arcuate nucleus (Arc) suggests that GHRH mRNA expression in this region might be directly regulated by Y2 receptors. Indeed, hypothalamic-specific deletion of Y2 receptors in conditional knockout mice prevented the fasting-induced reduction in Arc GHRH mRNA expression. On the other hand, fasting-induced decrease in GnRH mRNA expression in the medial preoptic area is more likely indirectly influenced by Y4 receptors because no Y4 receptors could be detected on GnRH neurons in this region. Together these data show that fasting inhibits the somatotropic axis via direct action on Y2 receptors in the Arc and indirectly inhibits the gonadotropic axis via Y4 receptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
148
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2056-65
pubmed:meshHeading
pubmed-meshheading:17272395-Animals, pubmed-meshheading:17272395-Arcuate Nucleus, pubmed-meshheading:17272395-Fasting, pubmed-meshheading:17272395-Gonads, pubmed-meshheading:17272395-Growth Hormone, pubmed-meshheading:17272395-Hypothalamo-Hypophyseal System, pubmed-meshheading:17272395-Leydig Cells, pubmed-meshheading:17272395-Male, pubmed-meshheading:17272395-Mice, pubmed-meshheading:17272395-Mice, Inbred C57BL, pubmed-meshheading:17272395-Mice, Knockout, pubmed-meshheading:17272395-Pituitary Gland, pubmed-meshheading:17272395-Preoptic Area, pubmed-meshheading:17272395-RNA, Messenger, pubmed-meshheading:17272395-Receptors, Neuropeptide, pubmed-meshheading:17272395-Receptors, Neuropeptide Y, pubmed-meshheading:17272395-Receptors, Pituitary Hormone-Regulating Hormone, pubmed-meshheading:17272395-Reproduction, pubmed-meshheading:17272395-Testis, pubmed-meshheading:17272395-Testosterone
pubmed:year
2007
pubmed:articleTitle
Fasting inhibits the growth and reproductive axes via distinct Y2 and Y4 receptor-mediated pathways.
pubmed:affiliation
Neuroscience Research Program, The Garvan Institute of Medical Research, Darlinghurst, New South Wales 2010, Sydney, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't