Linked Life Data

9568683

Source:http://linkedlifedata.com/resource/pubmed/id/9568683

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1998-5-7
pubmed:abstractText
In the rat, the glucagon-like peptide 1 (GLP-1)(7-36) amide inhibits neurones in the central nervous system responsible for food and water intake. GLP-1-induced inhibition of food intake may involve the hypothalamic arcuate nucleus, whereas rostral sensory circumventricular organs may be responsible for the inhibitory action of GLP-1 on drinking. To further investigate the role of these blood-brain-barrier-free areas in GLP-1-induced inhibition of ingestive behavior, neonatal Wistar rats were subjected to monosodium glutamate (MSG) treatment, which causes extensive damage to the arcuate nucleus as well as to parts of the sensory circumventricular organs. The inhibitory effect of GLP-1 on feeding induced by food deprivation was completely abolished in MSG-lesioned rats. This effect was not due to either a loss of sensitivity to anorectic agents or a loss of taste aversion because MSG-treated animals displayed normal anorectic responses to central administration of corticotropin-releasing factor and normal aversive responses to peripheral administration of both lithium chloride and D-amphetamine. In non-lesioned rats, neuropeptide Y (NPY)-induced feeding was significantly reduced by concomitant GLP-1 administration. In contrast, GLP-1 had no effect on NPY-induced feeding in MSG-lesioned rats, suggesting that the GLP-1 receptors that mediate inhibition of feeding are localized upstream to the NPY-sensitive neurones inducing feeding behavior. The inhibitory effect of GLP-1 on water intake was tested using an ANG II-elicited drinking paradigm. Central administration of GLP-1 inhibited ANG II drinking in both MSG-treated rats and their nontreated littermates. In contrast, peripheral administration of GLP-1 did not inhibit ANG II-induced drinking behavior in MSG-treated rats. Thus it is evident that centrally acting GLP-1 modulates feeding and drinking behavior via neurones sensitive to MSG lesioning in the arcuate nucleus and circumventricular organs, respectively.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
530-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9568683-Angiotensin II, pubmed-meshheading:9568683-Animals, pubmed-meshheading:9568683-Animals, Newborn, pubmed-meshheading:9568683-Arcuate Nucleus, pubmed-meshheading:9568683-Avoidance Learning, pubmed-meshheading:9568683-Blood Glucose, pubmed-meshheading:9568683-Blood-Brain Barrier, pubmed-meshheading:9568683-Brain, pubmed-meshheading:9568683-Cerebral Ventricles, pubmed-meshheading:9568683-Drinking, pubmed-meshheading:9568683-Eating, pubmed-meshheading:9568683-Food Additives, pubmed-meshheading:9568683-Food Deprivation, pubmed-meshheading:9568683-Glucagon, pubmed-meshheading:9568683-Glucagon-Like Peptide 1, pubmed-meshheading:9568683-Glucagon-Like Peptides, pubmed-meshheading:9568683-Male, pubmed-meshheading:9568683-Neuropeptide Y, pubmed-meshheading:9568683-Peptide Fragments, pubmed-meshheading:9568683-Rats, pubmed-meshheading:9568683-Rats, Wistar, pubmed-meshheading:9568683-Sodium Glutamate, pubmed-meshheading:9568683-Subfornical Organ, pubmed-meshheading:9568683-Taste
pubmed:year
1998
pubmed:articleTitle
Glucagon-like peptide 1(7-36) amide's central inhibition of feeding and peripheral inhibition of drinking are abolished by neonatal monosodium glutamate treatment.
pubmed:affiliation
Department of Medical Anatomy, University of Copenhagen, Denmark. m.tang@mai.ku.dk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't