Linked Life Data

3140678

Source:http://linkedlifedata.com/resource/pubmed/id/3140678

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4 Pt 2
pubmed:dateCreated
1988-11-9
pubmed:abstractText
Satiety appears to be mediated in part by neurally transmitted signals from the gastrointestinal tract. Capsaicin is a neurotoxin that selectively destroys small unmyelinated primary sensory neurons including some of those innervating the abdominal viscera. Therefore, we examined suppression of sham feeding induced by cholecystokinin octapeptide (CCK-8) or intraintestinal nutrient infusions in capsaicin-treated rats. Suppression of sham feeding induced by CCK-8 was significantly attenuated in rats treated with capsaicin. Suppression of sham feeding induced by intraintestinal infusions of maltose, oleic acid, or L-phenylalanine was also attenuated in capsaicin-treated rats. In contrast, capsaicin treatment did not attenuate the suppression of sham feeding induced by intraintestinal casein hydrolysate (mixed amino acids). Intraintestinal infusions of octanoic acid or D-phenylalanine solutions did not significantly suppress sham feeding in either vehicle- or capsaicin-treated rats. These results indicate that the suppression of feeding by some intestinal stimuli may be mediated by nutrient or peptide-sensitive visceral afferent neurons that are sensitive to damage or destruction by capsaicin.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
255
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R569-74
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Capsaicin attenuates suppression of sham feeding induced by intestinal nutrients.
pubmed:affiliation
Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, College of Veterinary Medicine, Washington State University, Pullman 99164.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.