Failure of 6-aminonicotinamide to inhibit the potentiating effect of leucine and arginine on glucose-induced insulin release in vitro

MacDonald, M. J. ; Ammon, H. P. T. ; Patel, T. ; Steinke, J.
Springer
Published 1974
ISSN:
1432-0428
Keywords:
Glucose ; 6-aminonicotinamide ; leucine ; arginine ; insulin release ; hexosemonophosphate pathway
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
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.
Type of Medium:
Electronic Resource
URL:
_version_ 1798295376137027584
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
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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