Linked Life Data

10824695

Source:http://linkedlifedata.com/resource/pubmed/id/10824695

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2000-8-10
pubmed:abstractText
The effects of oral administration of a synthetic trypsin inhibitor on bicarbonate secretion were examined in cholecystokinin A (CCK-A) receptor-deficient (OLETF) rats and compared with Wistar rats. Rats were fed chow containing 0.1% trypsin inhibitor for 7 days. Rats were prepared with cannulae draining bile and pancreatic juice separately and with duodenal and extrajugular vein cannulae after 3-day trypsin inhibitor ingestion. Then the animals were maintained in Bollman cages, and the experiments were conducted 4 days after surgery. After 1.5 h of basal secretion with bile-pancreatic juice return, bile-pancreatic juice was diverted for 2 h. The responses of bicarbonate secretion to bile-pancreatic juice diversion were significantly enhanced in rats treated with trypsin inhibitor compared with those given a control diet, whereas responses of fluid and protein secretion were not affected in OLETF rats. The response of protein secretion, but not those of fluid or bicarbonate secretion, was enhanced in Wistar rats by treatment with trypsin inhibitor. Carbonic anhydrase II gene expression was increased by 7-day treatment with trypsin inhibitor only in OLETF rats, and not in Wistar rats.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0885-3177
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
394-400
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Oral administration of a synthetic trypsin inhibitor increases pancreatic duct function in CCK-A receptor-deficient rats.
pubmed:affiliation
Department of Gastroenterology, National Kyushu Cancer Center, Fukuoka, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't