Na+ cotransport by metabolizable and nonmetabolizable amino acids stimulates a glucose-regulated insulin-secretory response

Neville McClenaghan, CR Barnett, Peter Flatt

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

The involvement of Na+ in insulin-secretory responses to metabolizable and nonmetabolizable amino acids known to be cotransported with Na+, were examined using islet-derived BRIN-BD11 cells. At stimulatory (16.7 mM) glucose, 10 mM of L-alanine, alpha-aminoisobutyric acid (AIB) or L-proline stimulated 1.3- to 10.4-fold (p <0.01) insulin-secretory responses. In each case, these effects were significantly greater than those observed at nonstimulatory (1.1 mM) glucose (p <0.01). While, tetrodotoxin blockade of voltage-dependent Na+ channels exerted no significant effect on insulin release, Na/K pump blockade with ouabain significantly promoted the amino acid-induced effects (p <0.05), Replacement of extracellular Na+ with equimolar N-methyl-D-glucamine(+) and omission of extracellular K+ or Ca2+ were all effective in removing the actions of each amino acid, confirming the critical role of ionic fluxes in the secretory responses to these amino acids. Collectively these results demonstrate that metabolizable and nonmetabolizable amino acids can induce glucose-dependent insulin-secretory responses by modulating electrogenic Na+ transport. (C) 1998 Academic Press.
LanguageEnglish
Pages299-303
JournalBiochemical and Biophysical Research Communications
Volume249
Issue number2
Publication statusPublished - Aug 1998

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Insulin
Amino Acids
Glucose
Tetrodotoxin
Ouabain
Proline
Alanine

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title = "Na+ cotransport by metabolizable and nonmetabolizable amino acids stimulates a glucose-regulated insulin-secretory response",
abstract = "The involvement of Na+ in insulin-secretory responses to metabolizable and nonmetabolizable amino acids known to be cotransported with Na+, were examined using islet-derived BRIN-BD11 cells. At stimulatory (16.7 mM) glucose, 10 mM of L-alanine, alpha-aminoisobutyric acid (AIB) or L-proline stimulated 1.3- to 10.4-fold (p <0.01) insulin-secretory responses. In each case, these effects were significantly greater than those observed at nonstimulatory (1.1 mM) glucose (p <0.01). While, tetrodotoxin blockade of voltage-dependent Na+ channels exerted no significant effect on insulin release, Na/K pump blockade with ouabain significantly promoted the amino acid-induced effects (p <0.05), Replacement of extracellular Na+ with equimolar N-methyl-D-glucamine(+) and omission of extracellular K+ or Ca2+ were all effective in removing the actions of each amino acid, confirming the critical role of ionic fluxes in the secretory responses to these amino acids. Collectively these results demonstrate that metabolizable and nonmetabolizable amino acids can induce glucose-dependent insulin-secretory responses by modulating electrogenic Na+ transport. (C) 1998 Academic Press.",
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Na+ cotransport by metabolizable and nonmetabolizable amino acids stimulates a glucose-regulated insulin-secretory response. / McClenaghan, Neville; Barnett, CR; Flatt, Peter.

In: Biochemical and Biophysical Research Communications, Vol. 249, No. 2, 08.1998, p. 299-303.

Research output: Contribution to journalArticle

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AB - The involvement of Na+ in insulin-secretory responses to metabolizable and nonmetabolizable amino acids known to be cotransported with Na+, were examined using islet-derived BRIN-BD11 cells. At stimulatory (16.7 mM) glucose, 10 mM of L-alanine, alpha-aminoisobutyric acid (AIB) or L-proline stimulated 1.3- to 10.4-fold (p <0.01) insulin-secretory responses. In each case, these effects were significantly greater than those observed at nonstimulatory (1.1 mM) glucose (p <0.01). While, tetrodotoxin blockade of voltage-dependent Na+ channels exerted no significant effect on insulin release, Na/K pump blockade with ouabain significantly promoted the amino acid-induced effects (p <0.05), Replacement of extracellular Na+ with equimolar N-methyl-D-glucamine(+) and omission of extracellular K+ or Ca2+ were all effective in removing the actions of each amino acid, confirming the critical role of ionic fluxes in the secretory responses to these amino acids. Collectively these results demonstrate that metabolizable and nonmetabolizable amino acids can induce glucose-dependent insulin-secretory responses by modulating electrogenic Na+ transport. (C) 1998 Academic Press.

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