Failure of 6-aminonicotinamide to inhibit the potentiating effect of leucine and arginine on glucose-induced insulin release in vitro
| ISSN: |
1432-0428
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| Keywords: |
Glucose ; 6-aminonicotinamide ; leucine ; arginine ; insulin release ; hexosemonophosphate pathway
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| Source: |
Springer Online Journal Archives 1860-2000
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| Topics: |
Medicine
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| Notes: |
Summary 6-aminonicotinamide (6-AN), which decreases the activity of the hexosemonophosphate pathway of pancreatic islets as well as the insulin releasing effect of glucose, was used to determine whether the potentiating effect of leucine and arginine on glucose induced insulin release is dependent upon normal function of the hexosemonophosphate pathway in pancreatic islets. In control islets, at low glucose concentrations (1 mg/ml), or in the absence of glucose, insulin release induced by these amino acids was negligible. At high glucose concentrations (3 mg/ml), which markedly stimulated insulin release (584 μU/5 islets/90 min), 1 and 10 mM leucine and 10 mM arginine increased insulin release by another 250 to 300 μU. Islets from animals treated with 6-AN released significantly less insulin in response to glucose alone or glucose plus leucine or arginine than control islets. However, the potentiating effect of these amino acids on insulin release from islets of animals treated with 6-AN was still similar to that observed in control islets and the total insulin released in the presence of 1 or 10 mM leucine or 10 mM arginine plus 3 mg/ml glucose was about the same as that observed in control islets in the presence of 3 mg/ml glucose alone. The data are consistent with the hypothesis that glucose exerts a permissive effect upon the insulinogenic actions of leucine and arginine, but that glucose oxidation through the hexosemonophosphate pathway is not important for the potentiation of glucose-induced insulin release by these amino acids.
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| Type of Medium: |
Electronic Resource
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| URL: |
| _version_ | 1798295376137027584 |
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| autor | MacDonald, M. J. Ammon, H. P. T. Patel, T. Steinke, J. |
| autorsonst | MacDonald, M. J. Ammon, H. P. T. Patel, T. Steinke, J. |
| book_url | http://dx.doi.org/10.1007/BF01219538 |
| datenlieferant | nat_lic_papers |
| hauptsatz | hsatz_simple |
| identnr | NLM199892016 |
| issn | 1432-0428 |
| journal_name | Diabetologia |
| materialart | 1 |
| notes | Summary 6-aminonicotinamide (6-AN), which decreases the activity of the hexosemonophosphate pathway of pancreatic islets as well as the insulin releasing effect of glucose, was used to determine whether the potentiating effect of leucine and arginine on glucose induced insulin release is dependent upon normal function of the hexosemonophosphate pathway in pancreatic islets. In control islets, at low glucose concentrations (1 mg/ml), or in the absence of glucose, insulin release induced by these amino acids was negligible. At high glucose concentrations (3 mg/ml), which markedly stimulated insulin release (584 μU/5 islets/90 min), 1 and 10 mM leucine and 10 mM arginine increased insulin release by another 250 to 300 μU. Islets from animals treated with 6-AN released significantly less insulin in response to glucose alone or glucose plus leucine or arginine than control islets. However, the potentiating effect of these amino acids on insulin release from islets of animals treated with 6-AN was still similar to that observed in control islets and the total insulin released in the presence of 1 or 10 mM leucine or 10 mM arginine plus 3 mg/ml glucose was about the same as that observed in control islets in the presence of 3 mg/ml glucose alone. The data are consistent with the hypothesis that glucose exerts a permissive effect upon the insulinogenic actions of leucine and arginine, but that glucose oxidation through the hexosemonophosphate pathway is not important for the potentiation of glucose-induced insulin release by these amino acids. |
| package_name | Springer |
| publikationsjahr_anzeige | 1974 |
| publikationsjahr_facette | 1974 |
| publikationsjahr_intervall | 8029:1970-1974 |
| publikationsjahr_sort | 1974 |
| publisher | Springer |
| reference | 10 (1974), S. 761-765 |
| schlagwort | Glucose 6-aminonicotinamide leucine arginine insulin release hexosemonophosphate pathway |
| search_space | articles |
| shingle_author_1 | MacDonald, M. J. Ammon, H. P. T. Patel, T. Steinke, J. |
| shingle_author_2 | MacDonald, M. J. Ammon, H. P. T. Patel, T. Steinke, J. |
| shingle_author_3 | MacDonald, M. J. Ammon, H. P. T. Patel, T. Steinke, J. |
| shingle_author_4 | MacDonald, M. J. Ammon, H. P. T. Patel, T. Steinke, J. |
| shingle_catch_all_1 | MacDonald, M. J. Ammon, H. P. T. Patel, T. Steinke, J. Failure of 6-aminonicotinamide to inhibit the potentiating effect of leucine and arginine on glucose-induced insulin release in vitro Glucose 6-aminonicotinamide leucine arginine insulin release hexosemonophosphate pathway Glucose 6-aminonicotinamide leucine arginine insulin release hexosemonophosphate pathway Summary 6-aminonicotinamide (6-AN), which decreases the activity of the hexosemonophosphate pathway of pancreatic islets as well as the insulin releasing effect of glucose, was used to determine whether the potentiating effect of leucine and arginine on glucose induced insulin release is dependent upon normal function of the hexosemonophosphate pathway in pancreatic islets. In control islets, at low glucose concentrations (1 mg/ml), or in the absence of glucose, insulin release induced by these amino acids was negligible. At high glucose concentrations (3 mg/ml), which markedly stimulated insulin release (584 μU/5 islets/90 min), 1 and 10 mM leucine and 10 mM arginine increased insulin release by another 250 to 300 μU. Islets from animals treated with 6-AN released significantly less insulin in response to glucose alone or glucose plus leucine or arginine than control islets. However, the potentiating effect of these amino acids on insulin release from islets of animals treated with 6-AN was still similar to that observed in control islets and the total insulin released in the presence of 1 or 10 mM leucine or 10 mM arginine plus 3 mg/ml glucose was about the same as that observed in control islets in the presence of 3 mg/ml glucose alone. The data are consistent with the hypothesis that glucose exerts a permissive effect upon the insulinogenic actions of leucine and arginine, but that glucose oxidation through the hexosemonophosphate pathway is not important for the potentiation of glucose-induced insulin release by these amino acids. 1432-0428 14320428 Springer |
| shingle_catch_all_2 | MacDonald, M. J. Ammon, H. P. T. Patel, T. Steinke, J. Failure of 6-aminonicotinamide to inhibit the potentiating effect of leucine and arginine on glucose-induced insulin release in vitro Glucose 6-aminonicotinamide leucine arginine insulin release hexosemonophosphate pathway Glucose 6-aminonicotinamide leucine arginine insulin release hexosemonophosphate pathway Summary 6-aminonicotinamide (6-AN), which decreases the activity of the hexosemonophosphate pathway of pancreatic islets as well as the insulin releasing effect of glucose, was used to determine whether the potentiating effect of leucine and arginine on glucose induced insulin release is dependent upon normal function of the hexosemonophosphate pathway in pancreatic islets. In control islets, at low glucose concentrations (1 mg/ml), or in the absence of glucose, insulin release induced by these amino acids was negligible. At high glucose concentrations (3 mg/ml), which markedly stimulated insulin release (584 μU/5 islets/90 min), 1 and 10 mM leucine and 10 mM arginine increased insulin release by another 250 to 300 μU. Islets from animals treated with 6-AN released significantly less insulin in response to glucose alone or glucose plus leucine or arginine than control islets. However, the potentiating effect of these amino acids on insulin release from islets of animals treated with 6-AN was still similar to that observed in control islets and the total insulin released in the presence of 1 or 10 mM leucine or 10 mM arginine plus 3 mg/ml glucose was about the same as that observed in control islets in the presence of 3 mg/ml glucose alone. The data are consistent with the hypothesis that glucose exerts a permissive effect upon the insulinogenic actions of leucine and arginine, but that glucose oxidation through the hexosemonophosphate pathway is not important for the potentiation of glucose-induced insulin release by these amino acids. 1432-0428 14320428 Springer |
| shingle_catch_all_3 | MacDonald, M. J. Ammon, H. P. T. Patel, T. Steinke, J. Failure of 6-aminonicotinamide to inhibit the potentiating effect of leucine and arginine on glucose-induced insulin release in vitro Glucose 6-aminonicotinamide leucine arginine insulin release hexosemonophosphate pathway Glucose 6-aminonicotinamide leucine arginine insulin release hexosemonophosphate pathway Summary 6-aminonicotinamide (6-AN), which decreases the activity of the hexosemonophosphate pathway of pancreatic islets as well as the insulin releasing effect of glucose, was used to determine whether the potentiating effect of leucine and arginine on glucose induced insulin release is dependent upon normal function of the hexosemonophosphate pathway in pancreatic islets. In control islets, at low glucose concentrations (1 mg/ml), or in the absence of glucose, insulin release induced by these amino acids was negligible. At high glucose concentrations (3 mg/ml), which markedly stimulated insulin release (584 μU/5 islets/90 min), 1 and 10 mM leucine and 10 mM arginine increased insulin release by another 250 to 300 μU. Islets from animals treated with 6-AN released significantly less insulin in response to glucose alone or glucose plus leucine or arginine than control islets. However, the potentiating effect of these amino acids on insulin release from islets of animals treated with 6-AN was still similar to that observed in control islets and the total insulin released in the presence of 1 or 10 mM leucine or 10 mM arginine plus 3 mg/ml glucose was about the same as that observed in control islets in the presence of 3 mg/ml glucose alone. The data are consistent with the hypothesis that glucose exerts a permissive effect upon the insulinogenic actions of leucine and arginine, but that glucose oxidation through the hexosemonophosphate pathway is not important for the potentiation of glucose-induced insulin release by these amino acids. 1432-0428 14320428 Springer |
| shingle_catch_all_4 | MacDonald, M. J. Ammon, H. P. T. Patel, T. Steinke, J. Failure of 6-aminonicotinamide to inhibit the potentiating effect of leucine and arginine on glucose-induced insulin release in vitro Glucose 6-aminonicotinamide leucine arginine insulin release hexosemonophosphate pathway Glucose 6-aminonicotinamide leucine arginine insulin release hexosemonophosphate pathway Summary 6-aminonicotinamide (6-AN), which decreases the activity of the hexosemonophosphate pathway of pancreatic islets as well as the insulin releasing effect of glucose, was used to determine whether the potentiating effect of leucine and arginine on glucose induced insulin release is dependent upon normal function of the hexosemonophosphate pathway in pancreatic islets. In control islets, at low glucose concentrations (1 mg/ml), or in the absence of glucose, insulin release induced by these amino acids was negligible. At high glucose concentrations (3 mg/ml), which markedly stimulated insulin release (584 μU/5 islets/90 min), 1 and 10 mM leucine and 10 mM arginine increased insulin release by another 250 to 300 μU. Islets from animals treated with 6-AN released significantly less insulin in response to glucose alone or glucose plus leucine or arginine than control islets. However, the potentiating effect of these amino acids on insulin release from islets of animals treated with 6-AN was still similar to that observed in control islets and the total insulin released in the presence of 1 or 10 mM leucine or 10 mM arginine plus 3 mg/ml glucose was about the same as that observed in control islets in the presence of 3 mg/ml glucose alone. The data are consistent with the hypothesis that glucose exerts a permissive effect upon the insulinogenic actions of leucine and arginine, but that glucose oxidation through the hexosemonophosphate pathway is not important for the potentiation of glucose-induced insulin release by these amino acids. 1432-0428 14320428 Springer |
| shingle_title_1 | Failure of 6-aminonicotinamide to inhibit the potentiating effect of leucine and arginine on glucose-induced insulin release in vitro |
| shingle_title_2 | Failure of 6-aminonicotinamide to inhibit the potentiating effect of leucine and arginine on glucose-induced insulin release in vitro |
| shingle_title_3 | Failure of 6-aminonicotinamide to inhibit the potentiating effect of leucine and arginine on glucose-induced insulin release in vitro |
| shingle_title_4 | Failure of 6-aminonicotinamide to inhibit the potentiating effect of leucine and arginine on glucose-induced insulin release in vitro |
| sigel_instance_filter | dkfz geomar wilbert ipn albert fhp |
| source_archive | Springer Online Journal Archives 1860-2000 |
| timestamp | 2024-05-06T09:35:13.307Z |
| titel | Failure of 6-aminonicotinamide to inhibit the potentiating effect of leucine and arginine on glucose-induced insulin release in vitro |
| titel_suche | Failure of 6-aminonicotinamide to inhibit the potentiating effect of leucine and arginine on glucose-induced insulin release in vitro |
| topic | WW-YZ |
| uid | nat_lic_papers_NLM199892016 |