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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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

McClenaghan NH,Barnett CR,Flatt PR

doi

10.1006/bbrc.1998.9136

subject

Has Abstract

pub_date

1998-08-19 00:00:00

pages

299-303

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(98)99136-7

journal_volume

249

pub_type

杂志文章

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