Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-7-21
pubmed:abstractText
The recent identification of loss-of-function mutations in the gene encoding GPR54, the receptor for the KiSS-1-derived peptides, kisspeptins, has highlighted a previously unrecognized pathway in the physiologic regulation of puberty and reproduction. Patients with loss-of-function mutations in GPR54 have idiopathic hypogonadotropic hypogonadism, and mice lacking GPR54 similarly fail to undergo puberty and have immature reproductive organs and low levels of sex steroids and gonadotropins. These observations have led to the hypothesis that kisspeptins activate hypothalamic GnRH release, thereby serving as a pivotal factor in the pubertal activation of the reproductive cascade. This hypothesis is supported by subsequent studies in rodent and primate models that have demonstrated localization of KiSS-1 mRNA in the hypothalamus, colocalization of GPR54 in GnRH neurons, GnRH-dependent activation of LH and FSH release by intracerebroventricular or peripheral administration of kisspeptin, and increased hypothalamic KiSS-1 and GPR54 mRNA levels at the onset of puberty. Taken together, these findings weave a compelling case for a role of the kisspeptin-GPR54 system in the activation of GnRH neurons at the time of pubertal awakening of the reproductive axis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1355-008X
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
277-84
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
KiSS-1 and GPR54 as new players in gonadotropin regulation and puberty.
pubmed:affiliation
Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. ukaiser@partners.org
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, N.I.H., Extramural