Linked Life Data

9744481

Source:http://linkedlifedata.com/resource/pubmed/id/9744481

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1998-12-4
pubmed:abstractText
Leptin has emerged as a major peripheral hormone, controlling central mechanisms of metabolism and related autonomic and endocrine functions. In the regulation of hypothalamic neurones, leptin is suggested to affect different second messenger systems and transcription regulating factors. The present study reports the predominant localization of leptin receptor immunoreactivity in the cis and trans cisternae of the Golgi apparatus in hypothalamic neuronal and glial cells. In these hypothalamic cells, translocation of leptin receptor immunoreactivity from the Golgi apparatus to the perikaryal membrane, nucleus or to the cytoplasm was not apparent after manipulation of the metabolic state either by fasting or suppression of the thyroid axis. On the other hand, leptin receptor immunoreactivity was associated with the perikaryal membrane of neurones in other parts of the central nervous system, including the dentate gyrus and the cingulate cortex. These data indicate an extremely high turnover of leptin receptors in hypothalamic target sites, but also raise the possibility that leptin may interact with the Golgi apparatus-related mechanisms to alter intracellular mechanisms.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0953-8194
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
647-50
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Leptin receptor immunoreactivity is associated with the Golgi apparatus of hypothalamic neurons and glial cells.
pubmed:affiliation
Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT 06520-8063, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.