Acute Exposure to a Precursor of Advanced Glycation End Products Induces a Dual Effect on the Rat Pancreatic Islet Function
Aim. Chronic diseases are the leading cause of death worldwide. Advanced glycation end products, known as AGEs, are a major risk factor for diabetes onset and maintenance. Methylglyoxal (MG), a highly reactive metabolite of glucose, is a precursor for the generation of endogenous AGEs. Methods. In t...
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| Format: | Article |
| Language: | English |
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Wiley
2014-01-01
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| Series: | International Journal of Endocrinology |
| Online Access: | http://dx.doi.org/10.1155/2014/378284 |
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| author | Ghada Elmhiri Luiz Felipe Barella Didier Vieau Sylvaine Camous Paulo C. F. Mathias Latifa Abdennebi-Najar |
| author_facet | Ghada Elmhiri Luiz Felipe Barella Didier Vieau Sylvaine Camous Paulo C. F. Mathias Latifa Abdennebi-Najar |
| author_sort | Ghada Elmhiri |
| collection | DOAJ |
| description | Aim. Chronic diseases are the leading cause of death worldwide. Advanced glycation end products, known as AGEs, are a major risk factor for diabetes onset and maintenance. Methylglyoxal (MG), a highly reactive metabolite of glucose, is a precursor for the generation of endogenous AGEs. Methods. In this current study we incubated in vitro pancreatic islets from adult rats in absence or presence of MG (10 μmol/l) with different concentrations of glucose and different metabolic components (acetylcholine, epinephrine, potassium, forskolin, and leucine). Results. Different effects of MG on insulin secretion were evidenced. In basal glucose stimulation (5.6 mM), MG induced a significant (P<0.05) increase of insulin secretion. By contrast, in higher glucose concentrations (8.3 mM and 16.7 mM), MG significantly inhibited insulin secretion (P<0.05). In the presence of potassium, forskolin, and epinephrine, MG enhanced insulin secretion (P<0.05), while when it was incubated with acetylcholine and leucine, MG resulted in a decrease of insulin secretion (P<0.05). Conclusion. We suggest that MG modulates the secretion activity of beta-cell depending on its level of stimulation by other metabolic factors. These results provide insights on a dual acute effect of MG on the pancreatic cells. |
| format | Article |
| id | doaj-art-3ff87ca2cfd547a881c4fade5af9d9a8 |
| institution | Kabale University |
| issn | 1687-8337 1687-8345 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Endocrinology |
| spelling | doaj-art-3ff87ca2cfd547a881c4fade5af9d9a82025-02-03T05:48:09ZengWileyInternational Journal of Endocrinology1687-83371687-83452014-01-01201410.1155/2014/378284378284Acute Exposure to a Precursor of Advanced Glycation End Products Induces a Dual Effect on the Rat Pancreatic Islet FunctionGhada Elmhiri0Luiz Felipe Barella1Didier Vieau2Sylvaine Camous3Paulo C. F. Mathias4Latifa Abdennebi-Najar5Institut Polytechnique LaSalle Beauvais, EGEAL-UP 2012.10.101., 19 rue Pierre Waguet, 60026 Beauvais Cedex, FranceLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, 87020-900 Maringá, PR, BrazilEnvironnement Périnatal et Croissance (EA4489), Equipe Dénutritions Maternelles Périnatales, SN4, Université de Lille 1, 59655 Villeneuve d’Ascq, FranceINRA, UMR1198, Biologie du Développement et Reproduction, 78352 Jouy en Josas, FranceLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, 87020-900 Maringá, PR, BrazilInstitut Polytechnique LaSalle Beauvais, EGEAL-UP 2012.10.101., 19 rue Pierre Waguet, 60026 Beauvais Cedex, FranceAim. Chronic diseases are the leading cause of death worldwide. Advanced glycation end products, known as AGEs, are a major risk factor for diabetes onset and maintenance. Methylglyoxal (MG), a highly reactive metabolite of glucose, is a precursor for the generation of endogenous AGEs. Methods. In this current study we incubated in vitro pancreatic islets from adult rats in absence or presence of MG (10 μmol/l) with different concentrations of glucose and different metabolic components (acetylcholine, epinephrine, potassium, forskolin, and leucine). Results. Different effects of MG on insulin secretion were evidenced. In basal glucose stimulation (5.6 mM), MG induced a significant (P<0.05) increase of insulin secretion. By contrast, in higher glucose concentrations (8.3 mM and 16.7 mM), MG significantly inhibited insulin secretion (P<0.05). In the presence of potassium, forskolin, and epinephrine, MG enhanced insulin secretion (P<0.05), while when it was incubated with acetylcholine and leucine, MG resulted in a decrease of insulin secretion (P<0.05). Conclusion. We suggest that MG modulates the secretion activity of beta-cell depending on its level of stimulation by other metabolic factors. These results provide insights on a dual acute effect of MG on the pancreatic cells.http://dx.doi.org/10.1155/2014/378284 |
| spellingShingle | Ghada Elmhiri Luiz Felipe Barella Didier Vieau Sylvaine Camous Paulo C. F. Mathias Latifa Abdennebi-Najar Acute Exposure to a Precursor of Advanced Glycation End Products Induces a Dual Effect on the Rat Pancreatic Islet Function International Journal of Endocrinology |
| title | Acute Exposure to a Precursor of Advanced Glycation End Products Induces a Dual Effect on the Rat Pancreatic Islet Function |
| title_full | Acute Exposure to a Precursor of Advanced Glycation End Products Induces a Dual Effect on the Rat Pancreatic Islet Function |
| title_fullStr | Acute Exposure to a Precursor of Advanced Glycation End Products Induces a Dual Effect on the Rat Pancreatic Islet Function |
| title_full_unstemmed | Acute Exposure to a Precursor of Advanced Glycation End Products Induces a Dual Effect on the Rat Pancreatic Islet Function |
| title_short | Acute Exposure to a Precursor of Advanced Glycation End Products Induces a Dual Effect on the Rat Pancreatic Islet Function |
| title_sort | acute exposure to a precursor of advanced glycation end products induces a dual effect on the rat pancreatic islet function |
| url | http://dx.doi.org/10.1155/2014/378284 |
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