Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2008-5-21
pubmed:abstractText
We recently reported that the hypothalamic homeobox domain transcription factor Bsx plays an essential role in the central nervous system control of spontaneous physical activity and the generation of hyperphagic responses. Moreover, we found Bsx to be a master regulator for the hypothalamic expression of key orexigenic neuropeptide Y and agouti gene-related protein. We now hypothesized that Bsx, which is expressed in the dorsomedial and arcuate nucleus (ARC) of the hypothalamus, is regulated by afferent signals in response to peripheral energy balance. Bsx expression was analyzed using in situ hybridization in fed vs. fasted (24 h) and ghrelin vs. leptin-treated rats, as well as in mice deficient for leptin or the ghrelin signaling. Ghrelin administration increased, whereas ghrelin receptor antagonist decreased ARC Bsx expression. Leptin injection attenuated the fasting-induced increase in ARC Bsx levels but had no effect in fed rats. Dorsomedial hypothalamic nucleus Bsx expression was unaffected by pharmacological modifications of leptin or ghrelin signaling. Obese leptin-deficient (ob/ob) mice, but not obese melanocortin 4 receptor-knockout mice, showed higher expression of Bsx, consistent with dependency from afferent leptin rather than increased adiposity per se. Interestingly, exposure to a high-fat diet triggered Bsx expression, consistent with the concept that decreased leptin signaling due to a high-fat diet induced leptin resistance. Our data indicate that ARC Bsx expression is specifically regulated by afferent energy balance signals, including input from leptin and ghrelin. Future studies will be necessary to test if Bsx may be involved in the pathogenesis of leptin resistance.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-11057670, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-11196643, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-11373681, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-12077332, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-12597862, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-12933644, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-14678827, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-14726256, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-15207242, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-15856065, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-16099943, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-16158063, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-16210868, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-16251950, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-16254186, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-16322794, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-16322795, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-16644689, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-17339026, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-17448988, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-17550780, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-17885689, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-7984236, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-8603777, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-8632796, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-8939859, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-9202122, http://linkedlifedata.com/resource/pubmed/commentcorrection/18308842-9927310
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
149
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3009-15
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Bsx, a novel hypothalamic factor linking feeding with locomotor activity, is regulated by energy availability.
pubmed:affiliation
Department of Psychiatry, Obesity Research Center, University of Cincinnati, Cincinnati, Ohio 45237, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural