Linked Life Data

20389091

Source:http://linkedlifedata.com/resource/pubmed/id/20389091

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2010-4-14
pubmed:abstractText
The hypothalamus integrates multiple environmental and developmental cues relevant to reproductive function, serving to transduce these into a pulsatile output of gonadotropin-releasing hormone (GnRH). Although neuroanatomical and physiological studies have yielded key clues about the functional organisation of the so-called 'GnRH pulse generator', only in the last decade have the molecular components of the circuitry upstream from GnRH begun to be elucidated. A major contributor to this has been human genetics, through identification of mutations causing isolated hypogonadotropic hypogonadism (IHH) without developmental defects. The greatest success of this approach was the finding in 2003 that mutations of KISS1R cause IHH, producing a quantum leap in understanding of regulation of GnRH secretion, and energising the field. New evidence has now emerged that loss of function of neurokinin B (NKB) or its receptor, the neurokinin-3 receptor, produces IHH of similar severity to that caused by KISS1R mutations in humans. Preliminary evidence suggests that the role of NKB in reproductive function differs significantly between humans and rodents, posing challenges for future studies. We review the human genetics of NKB and its receptor, and discuss the future work required to elucidate their precise role in the regulation of human GnRH secretion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1662-3762
pubmed:author
pubmed:copyrightInfo
Copyright 2010 S. Karger AG, Basel.
pubmed:issnType
Electronic
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
133-41
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Neurokinin B and its receptor in hypogonadotropic hypogonadism.
pubmed:affiliation
University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, UK. rks16@cam.ac.uk
pubmed:publicationType
Journal Article, Review