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   <dc:title>Gastrin treatment stimulates beta cell regeneration and improves glucose tolerance in 95% pancreatectomized rats</dc:title>
   <dc:creator>Téllez i Besolí, Noèlia</dc:creator>
   <dc:creator>Joanny Ordóñez, Géraldine</dc:creator>
   <dc:creator>Escoriza, Jessica</dc:creator>
   <dc:creator>Vilaseca Barceló, Marina</dc:creator>
   <dc:creator>Montanya Mias, Eduard</dc:creator>
   <dc:subject>Gastrina</dc:subject>
   <dc:subject>Cèl·lules B</dc:subject>
   <dc:subject>Glucosa</dc:subject>
   <dc:subject>Tolerància</dc:subject>
   <dc:subject>Ús terapèutic</dc:subject>
   <dc:subject>Gastrin</dc:subject>
   <dc:subject>B cells</dc:subject>
   <dc:subject>Glucose</dc:subject>
   <dc:subject>Toleration</dc:subject>
   <dc:subject>Therapeutic use</dc:subject>
   <dc:description>β-Cell mass reduction is a central aspect in the development of type 1 and type 2 diabetes, and substitution or regeneration of the lost β-cells is a potentially curative treatment of diabetes. To study the effects of gastrin on β-cell mass in rats with 95% pancreatectomy (95%-Px), a model of pancreatic regeneration, rats underwent 95% Px or sham Px and were treated with [15 leu] gastrin-17 (Px+G and S+G) or vehicle (Px+V and S+V) for 15 d. In 95% Px rats, gastrin treatment reduced hyperglycemia (280 ± 52 mg vs. 436 ± 51 mg/dl, P &lt; 0.05), and increased β-cell mass (1.15 ± 0.15 mg)) compared with vehicle-treated rats (0.67 ± 0.15 mg, P &lt; 0.05). Gastrin treatment induced β-cell regeneration by enhancing β-cell neogenesis (increased number of extraislet β-cells in Px+G: 0.42 ± 0.05 cells/mm(2) vs. Px+V: 0.27 ± 0.07 cells/mm(2), P &lt; 0.05, and pancreatic and duodenal homeobox 1 expression in ductal cells of Px+G: 1.21 ± 0.38% vs. Px+V: 0.23 ± 0.10%, P &lt; 0.05) and replication (Px+G: 1.65 ± 0.26% vs. S+V: 0.64 ± 0.14%; P &lt; 0.05). In addition, reduced β-cell apoptosis contributed to the increased β-cell mass in gastrin-treated rats (Px+G: 0.07 ± 0.02%, Px+V: 0.23 ± 0.05%; P &lt; 0.05). Gastrin action on β-cell regeneration and survival increased β-cell mass and improved glucose tolerance in 95% Px rats, supporting a potential role of gastrin in the treatment of diabetes.</dc:description>
   <dc:date>2019-06-03T14:08:16Z</dc:date>
   <dc:date>2019-06-03T14:08:16Z</dc:date>
   <dc:date>2011-07</dc:date>
   <dc:date>2019-06-03T14:08:17Z</dc:date>
   <dc:type>info:eu-repo/semantics/article</dc:type>
   <dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
   <dc:identifier>0013-7227</dc:identifier>
   <dc:identifier>https://hdl.handle.net/2445/134421</dc:identifier>
   <dc:identifier>602773</dc:identifier>
   <dc:identifier>21558313</dc:identifier>
   <dc:language>eng</dc:language>
   <dc:relation>Reproducció del document publicat a: https://doi.org/10.1210/en.2011-0066</dc:relation>
   <dc:relation>Endocrinology, 2011, vol. 152, num. 7, p. 2580-2588</dc:relation>
   <dc:relation>https://doi.org/10.1210/en.2011-0066</dc:relation>
   <dc:rights>(c) Association for the Study of Internal Secretions, 2011</dc:rights>
   <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
   <dc:format>9 p.</dc:format>
   <dc:format>application/pdf</dc:format>
   <dc:format>application/pdf</dc:format>
   <dc:publisher>Association for the Study of Internal Secretions</dc:publisher>
   <dc:source>Articles publicats en revistes (Ciències Clíniques)</dc:source>
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