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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4 Pt 2
pubmed:dateCreated
1989-11-17
pubmed:abstractText
Cholecystokinin octapeptide, administered into the third cerebral ventricle (icv), suppresses feeding in sheep, pigs, chicken, rats, and dogs. Because of the species differences in the feeding response to cholecystokinin (CCK), we studied the pharmacological characterization of this peptide on feeding in 16-h-fasted dogs. We examined the effects of CCK-(26-33)-NH2 (CCK-8) and a variety of its analogues, nonsulfated CCK-(26-33)-NH2 (desulfated CCK-8), CCK-(26-33)-OH (deamidated CCK-8), (Nle28,31)-CCK-(26-33)-NH2 [(Nle28,31)-CCK-8], succinyl-CCK-(27-33)-NH2 (Suc-CCK-7) succinyl-Thr28, Leu29, MePhe33-CCK-(27-33)-NH2 [Suc-Thr28, Leu29, MePhe33)-CCK-7], CCK-(29-33)-NH2 (CCK-5), and CCK-(30-33)-NH2 (CCK-4) on food intake after iv injection. Systemic dose-response studies appeared to reveal the following rank order of potencies: Suc-CCK-7 = Suc-(Thr28, Leu29, MePhe33)-CCK-7 greater than CCK-8 = (Nle28,31)-CCK-8 greater than desulfated CCK-8 greater than deaminated CCK-8 greater than CCK-5 = CCK-4 = 0. Smaller COOH-terminal fragments acted as antagonists to the satiety effects of CCK-8. These data demonstrate in the dog that the structural requirements for the behavioral activity of CCK-8 are the COOH-terminal amide group, the sulfate ester of the tyrosine moiety, and the conformational constraints observed in CCK-7.
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
257
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R946-51
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Effect of cholecystokinin octapeptide analogues on food intake in the dog.
pubmed:affiliation
Second Department of Internal Medicine, Kobe University School of Medicine, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't