Endocrine Journal
Online ISSN : 1348-4540
Print ISSN : 0918-8959
ISSN-L : 0918-8959
Sphingosine 1-Phosphate Stimulates Insulin Secretion in HIT-T 15 Cells and Mouse Islets
HIROYUKI SHIMIZUFUMIKAZU OKAJIMATAKAO KIMURAKEN-ICHI OHTANITAKAHUMI TSUCHIYAHIROKI TAKAHASHIATSUSHI KUWABARAHIDEAKI TOMURAKOICHI SATOMASATOMO MORI
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2000 Volume 47 Issue 3 Pages 261-269

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Abstract

Sphingosine is involved in the regulation of cellular processes as a second messenger in various kinds of cells. Since the possible involvement of sphingosine has not been investigated in pancreatic β-cells, we determined the expression of putative sphingosine 1-phosphate (S1P) receptors and the effect of sphingosine on pancreatic β-cell function using a clonal Hamster β-cell line, HIT-T 15 cells and isolated mouse islets. We showed the expression of putative S1P receptors, Edg-3 and AGR16/H218 in HIT-T 15 cells. Ten and 20μM S1P significantly stimulated insulin secretion for 10 minutes in HIT-T 15 cells. Ten μM S1P significantly increased insulin secretion from isolated mouse islets. Ten μM S1P obviously increased intracellular Ca2+ concentration ([Ca2+]i). Fifty nM nifedipine did not affect the S1P stimulation of insulin secretion in HIT-T 15 cells. Two μM U73122 (phospholipase C inhibitor) completely deleted 10μM S1P-induced stimulation of insulin secretion for 10 minutes, but U73343 (an inactive analogue of U73122) did not. S1P dose-dependently inhibited intracellular cyclic AMP levels. Pretreatment with 100ng/ml pertussis toxin (PTX) partially, but significantly attenuated an increase of insulin secretion by 10μM S1P. These data suggested that PTX-sensitive G-protein-dependent pathway may, at least in part, be involved in an increase of non-glucose stimulated insulin secretion by S1P through the activation of phospholipase C- Ca2+ system.

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© The Japan Endocrine Society
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