دورية أكاديمية
The atrial natriuretic peptide and guanylyl cyclase-A system modulates pancreatic beta-cell function
العنوان: | The atrial natriuretic peptide and guanylyl cyclase-A system modulates pancreatic beta-cell function |
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المؤلفون: | Ropero, Ana B., Soriano, Sergi, Tudurí, Eva, Marroquí, Laura, Téllez i Besolí, Noèlia, Gassner, Birgit, Juan-Picó, Pablo, Montanya Mias, Eduard, Quesada, Ivan, Kuhn, Michaela, Nadal, Angel |
المصدر: | Articles publicats en revistes (Ciències Clíniques) |
بيانات النشر: | Association for the Study of Internal Secretions |
سنة النشر: | 2010 |
المجموعة: | Dipòsit Digital de la Universitat de Barcelona |
مصطلحات موضوعية: | Fisiologia, Secreció, Insulina, Pèptids, Physiology, Secretion, Insulin, Peptides |
الوصف: | Atrial natriuretic peptide (ANP) and its guanylyl cyclase-A (GC-A) receptor are being involved in metabolism, although their role in the endocrine pancreas is still greatly unknown. The aim of this work is to study a possible role for the ANP/GC-A system in modulating pancreatic beta-cell function. The results presented here show a direct effect of the GC-A receptor in regulating glucose-stimulated insulin secretion (GSIS) and beta-cell mass. GC-A activation by its natural ligand, ANP, rapidly blocked ATP-dependent potassium (K(ATP)) channel activity, increased glucose-elicited Ca(2+) signals, and enhanced GSIS in islets of Langerhans. The effect in GSIS was inhibited in islets from GC-A knockout (KO) mice. Pancreatic islets from GC-A KO mice responded to increasing glucose concentrations with enhanced insulin secretion compared with wild type (WT). Remarkably, islets from GC-A KO mice were smaller, presented lower beta-cell mass and decreased insulin content. However, glucose-induced Ca(2+) response was more vigorous in GC-A KO islets, and basal K(ATP) channel activity in GC-A KO beta-cells was greatly diminished compared with WT. When protein levels of the two K(ATP) channel constitutive subunits sulfonylurea receptor 1 and Inward rectifier potassium channel 6.2 were measured, both were diminished in GC-A KO islets. These alterations on beta-cell function were not associated with disruption of glucose tolerance or insulin sensitivity in vivo. Glucose and insulin tolerance tests were similar in WT and GC-A KO mice. Our data suggest that the ANP/GC-A system may have a modulating effect on beta-cell function. |
نوع الوثيقة: | article in journal/newspaper |
وصف الملف: | 10 p.; application/pdf |
اللغة: | English |
تدمد: | 0013-7227 |
العلاقة: | Reproducció del document publicat a: https://doi.org/10.1210/en.2010-0119Test; Endocrinology, 2010, vol. 151, num. 8, p. 3665-3674; https://doi.org/10.1210/en.2010-0119Test; http://hdl.handle.net/2445/134299Test; 630888 |
الإتاحة: | https://doi.org/10.1210/en.2010-0119Test http://hdl.handle.net/2445/134299Test |
حقوق: | (c) Association for the Study of Internal Secretions, 2010 ; info:eu-repo/semantics/openAccess |
رقم الانضمام: | edsbas.9D0BEEC3 |
قاعدة البيانات: | BASE |
تدمد: | 00137227 |
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