Somatostatin binding capacity, guanylate cyclase and tyrosine phosphatase activities during pancreatic proliferation in the rat induced by gastrectomy
Authors
Rodríguez Martín, Eulalia; Valencia Torralba, Ana M.; Colás Escudero, María Begoña; García Escribano, Carmen; Rodríguez Puyol, Manuel; [et al.]Identifiers
Permanent link (URI): http://hdl.handle.net/10017/2318DOI: 10.1016/0196-9781(95)02023-3
ISSN: 0196-9781
Publisher
Elsevier
Date
1995Funders
Ministerio de Educación y Ciencia
Bibliographic citation
Peptides, 1995, v. 16, n. 8, p. 1461-1467
Keywords
Gastrectomy
Guanylate cyclase
Somatostatin receptors
Pancreatic acinar membranes
Somatostatin like-immunoreactivity
Rat
Project
info:eu-repo/grantAgreement/MEC//PB94-0339/ES//
Document type
info:eu-repo/semantics/article
Version
info:eu-repo/semantics/publishedVersion
Publisher's version
http://dx.doi.org/10.1016/0196-9781(95)02023-3Rights
(c) Elsevier, 1995
Access rights
info:eu-repo/semantics/openAccess
Abstract
Gastrectomy increased pancreatic growth and this effect was associated with an increase in the number of somatostatin-14 (SS) receptors (146% of control) without altering their affinity. SS increased guanylate cyclase activity twofold in pancreatic acinar membranes from gastrectomized rats. The gastrectomy decreased pancreatic SS-like immunoreactivity (SS-LI) content (55% of control levels) and tyrosine phosphatase activity (74% of control levels). Administration of proglumide (20 mg/kg, IF), a gastrin/cholecystokinin (CCK) receptor antagonist, suppressed the inhibitory effect of gastrectomy on basal tyrosine phosphatase activity and SS-LI content, which returned to control levels. Furthermore, proglumide suppressed the increase of the number of SS receptors and of SS-stimulated guanylate cyclase activity induced by gastrectomy. All this suggests that pancreatic acinar cell growth is associated with upregulation of SS receptors, which could represent a mechanism promoted by the cell to negatively regulate the mitogenic activity of pancreatic growth factors such as CCK. In addition, the results also suggest that the negative regulation of tyrosine phosphatase activity may be important in the events involved in the pancreatic hyperplasia observed after gastrectomy.
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