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Titolo:
Pancreatic function in CCK-deficient mice: adaptation to dietary protein does not require CCK
Autore:
Lacourse, KA; Swanberg, LJ; Gillespie, PJ; Rehfeld, JF; Saunders, TL; Samuelson, LC;
Indirizzi:
Univ Michigan, Dept Physiol, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 ept Physiol, Ann Arbor, MI 48109 USA Rigshosp, Dept Clin Biochem, DK-2100 Copenhagen, Denmark Rigshosp Copenhagen Denmark DK-2100 Biochem, DK-2100 Copenhagen, Denmark
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
fascicolo: 5, volume: 39, anno: 1999,
pagine: G1302 - G1309
SICI:
0193-1857(199905)39:5<G1302:PFICMA>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHOLECYSTOKININ RECEPTOR ANTAGONIST; EMBRYONIC STEM-CELLS; RAT PANCREAS; SHORT-TERM; GROWTH; SECRETION; SOMATOSTATIN; AMYLASE; CERULEIN; INSULIN;
Keywords:
gastrointestinal hormones; knockout mice; acinar cells; digestive enzymes; pancreatic hypertrophy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Samuelson, LC Univ Michigan, Dept Physiol, 7761 Med Sci 2, Ann Arbor, MI 48109 USA Univ Michigan 7761 Med Sci 2 Ann Arbor MI USA 48109 8109 USA
Citazione:
K.A. Lacourse et al., "Pancreatic function in CCK-deficient mice: adaptation to dietary protein does not require CCK", AM J P-GAST, 39(5), 1999, pp. G1302-G1309

Abstract

A CCK-deficient mouse mutant generated by gene targeting in embryonic stemcells was analyzed to determine the importance of CCK for growth and function of the exocrine pancreas and for pancreatic adaptation to dietary changes. RIAs confirmed the absence of CCK in mutant mice and demonstrated that tissue concentrations of the related peptide gastrin were normal. CCK-deficient mice are viable and fertile and exhibit normal body weight. Pancreas weight and cellular morphology appeared normal, although pancreatic amylase content was elevated in CCK-deficient mice. We found that a high-protein diet increased pancreatic weight, protein, DNA, and chymotrypsinogen content;similarly in CCK-deficient and wild-type mice. This result demonstrates that CCK is not required for protein-induced pancreatic hypertrophy and increased proteolytic enzyme content. This is a novel finding, since CCK has been considered the primary mediator of dietary protein-induced changes in thepancreas. Altered somatostatin concentrations in brain and duodenum of CCK-deficient mice suggest that other regulatory pathways are modified to compensate far the CCK deficiency.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 14:08:58