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Titolo:
Acid inhibition by intestinal nutrients mediated by CCK-A receptors but not plasma CCK
Autore:
Lloyd, KCK; Wang, JF; Solomon, TE;
Indirizzi:
Univ Calif Davis, Ctr Comparat Med, Sch Vet Med, Dept Anat Physiol & Cell Biol, Davis, CA 95616 USA Univ Calif Davis Davis CA USA 95616 siol & Cell Biol, Davis, CA 95616 USA Vet Affairs Greater Los Angeles Healthcare Syst, Digest Dis Res Ctr, CURE,Los Angeles, CA 90073 USA Vet Affairs Greater Los Angeles Healthcare Syst Los Angeles CA USA 90073 Univ Calif Los Angeles, Sch Med, Div Digest Dis, Los Angeles, CA 90024 USAUniv Calif Los Angeles Los Angeles CA USA 90024 Los Angeles, CA 90024 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
fascicolo: 4, volume: 281, anno: 2001,
pagine: G924 - G930
SICI:
0193-1857(200110)281:4<G924:AIBINM>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
STIMULATED GASTRIC-ACID; FOS PROTEIN EXPRESSION; FAT-INDUCED INHIBITION; SOLITARY TRACT; PEPTIDE-YY; BRAIN-STEM; OLEIC-ACID; AWAKE RATS; CHOLECYSTOKININ; SECRETION;
Keywords:
gastric acid secretion; enterogastrone; intestinal phase; cholecystokinin; peptone meal;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Lloyd, KCK Univ Calif Davis, Ctr Comparat Med, Sch Vet Med, Dept Anat Physiol & Cell Biol, 1 Shields Ave, Davis, CA 95616 USA Univ Calif Davis 1 Shields Ave Davis CA USA 95616 CA 95616 USA
Citazione:
K.C.K. Lloyd et al., "Acid inhibition by intestinal nutrients mediated by CCK-A receptors but not plasma CCK", AM J P-GAST, 281(4), 2001, pp. G924-G930

Abstract

We examined the role of CCK-A receptors in acid inhibition by intestinal nutrients. Gastric acid and plasma CCK and gastrin levels were measured in rats with gastric and duodenal fistulas during intragastric 8% peptone and duodenal perfusion with saline, complete liquid diet (CLD; 20% carbohydrate,6% fat, and 5% protein), and the individual components of CLD. Acid outputwas significantly inhibited (50-60%) by CLD, lipid, and dextrose. Plasma CCK was significantly increased by CLD (from 2.6 +/-0.3 to 4.8 +/-0.5 pM) and lipid (4.6 +/-0.5 pM). CCK levels 50-fold higher (218 +/- 33 pM) were required to achieve similar acid inhibition by exogenous CCK-8 (10 nmol.kg(-1).h(-1) iv). Intestinal soybean trypsin inhibitor elevated CCK (10.9 +/-2.5 pM) without inhibiting acid secretion. The CCK-A antagonist MK-329 (1 mg/kgiv) reversed acid inhibition caused by CLD, lipid, and dextrose. Peptone-stimulated gastrin (21.7 +/-1.9 pM) was significantly inhibited by CLD (14.5+/-3.6 pM), lipid (12.3 +/-2.2 pM), and dextrose (11.9 +/-1.5 pM). Lipid and carbohydrate inhibit acid secretion by activating CCK-A receptors but not by altering plasma CCK concentrations.

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Documento generato il 30/03/20 alle ore 20:01:51