Linked Life Data

10433218

Source:http://linkedlifedata.com/resource/pubmed/id/10433218

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1999-8-17
pubmed:abstractText
We reported previously an increase in leptin receptor (OBR) gene expression in the anterior pituitary of human GH-releasing hormone (hGHRH) transgenic mice. The primary goal of this study was to investigate the possible mechanisms regulating OBR expression in these mice. Compared with normal sibling controls, hGHRH transgenic mice had significantly greater amounts of abdominal fat, higher levels of leptin messenger RNA (mRNA), and a 2-fold increase in plasma leptin concentrations. Despite normal plasma glucose levels, hGHRH transgenic mice had 4.5-fold elevated levels of plasma insulin. Using a ribonuclease protection assay, we measured the mRNA levels of the OBR long form (OBR(L)) in the anterior pituitary and hypothalamus after 48 h of fasting. In the anterior pituitary, food deprivation induced dramatic increases in OBR(L) mRNA levels in both normal and transgenic mice. In contrast, in the hypothalamus, fasting resulted in a significant decrease in OBR(L) gene expression in normal mice, and no changes were detected in hGHRH transgenic mice. Using dual in situ hybridization, OBR(L) mRNA was detected in somatotrophs. Moreover, the number of OBR(L)-positive pituitary cells as well as the percentage of OBR(L)-positive cells that express GH mRNA were increased in transgenic mice. In conclusion, 1) the modest obesity in hGHRH transgenic mice is associated with increases in leptin synthesis and secretion as well as insulin secretion; 2) GH and/or GHRH as well as leptin and insulin may differentially contribute to the changes in OBR(L) gene expression in the anterior pituitary and the hypothalamus; 3) the response of OBR(L) gene expression in the hypothalamus to fasting is absent in the modestly obese hGHRH transgenic mice; and 4) somatotrophs are target cells for leptin, and the increase in OBR(L) gene expression in the pituitary of hGHRH transgenic mice is due at least in part to the increase in the number of cells expressing OBR(L).
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
140
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3609-14
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:10433218-Adipose Tissue, pubmed-meshheading:10433218-Animals, pubmed-meshheading:10433218-Carrier Proteins, pubmed-meshheading:10433218-Fasting, pubmed-meshheading:10433218-Gene Expression Regulation, pubmed-meshheading:10433218-Growth Hormone-Releasing Hormone, pubmed-meshheading:10433218-Humans, pubmed-meshheading:10433218-Hypothalamus, pubmed-meshheading:10433218-Male, pubmed-meshheading:10433218-Mice, pubmed-meshheading:10433218-Mice, Transgenic, pubmed-meshheading:10433218-Obesity, pubmed-meshheading:10433218-Organ Specificity, pubmed-meshheading:10433218-Pituitary Gland, Anterior, pubmed-meshheading:10433218-RNA, Messenger, pubmed-meshheading:10433218-Receptors, Cell Surface, pubmed-meshheading:10433218-Receptors, Leptin, pubmed-meshheading:10433218-Reference Values, pubmed-meshheading:10433218-Transcription, Genetic
pubmed:year
1999
pubmed:articleTitle
The human growth hormone-releasing hormone transgenic mouse as a model of modest obesity: differential changes in leptin receptor (OBR) gene expression in the anterior pituitary and hypothalamus after fasting and OBR localization in somatotrophs.
pubmed:affiliation
Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington 40536-0084, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't