Somatostatin binding capacity, guanylate cyclase and tyrosine phosphatase activities during pancreatic proliferation in the rat induced by gastrectomy

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 gast...

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Bibliographic Details
Authors: Rodríguez Martín, Eulalia, Valencia Torralba, Ana M., Colás Escudero, María Begoña|||0000-0001-7913-3006, García Escribano, Carmen, Rodríguez Puyol, Manuel Antonio|||0000-0002-5230-6664, Susini, Christiane, Arilla Ferreiro, Eduardo
Format: article
Publication Date:1995
Country:España
Institution:Universidad de Alcalá (UAH)
Repository:e_Buah Biblioteca Digital Universidad de Alcalá
Language:English
OAI Identifier:oai:ebuah.uah.es:10017/2318
Online Access:http://hdl.handle.net/10017/2318
https://dx.doi.org/10.1016/0196-9781(95)02023-3
Access Level:Open access
Keyword:Gastrectomy
Guanylate cyclase
Somatostatin receptors
Pancreatic acinar membranes
Somatostatin like-immunoreactivity
Rat
Bioquímica
Ciencia
Biochemistry
Science
Description
Summary: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.