Sphingosine 1-Phosphate Stimulates Insulin Secretion in HIT-T 15 Cells and Mouse Islets.

Accession number;00A0626830
Title;Sphingosine 1-Phosphate Stimulates Insulin Secretion in HIT-T 15 Cells and Mouse Islets.
Author;SHIMIZU H(Gunma Univ. School Of Medicine, Gunma, Jpn)   OKAJIMA F(Gunma Univ., Gunma, Jpn)   KIMURA T(Gunma Univ. School Of Medicine, Gunma, Jpn)   OHTANI K(Gunma Univ. School Of Medicine, Gunma, Jpn)   TSUCHIYA T(Gunma Univ. School Of Medicine, Gunma, Jpn)   KUWABARA H(Gunma Univ. School Of Medicine, Gunma, Jpn)   TOMURA H(Gunma Univ., Gunma, Jpn)   SATO K(Gunma Univ., Gunma, Jpn)   MORI M(Gunma Univ. School Of Medicine, Gunma, Jpn)   
Journal Title;Endocr J
Journal Code:F0625A
ISSN:0918-8959
VOL.47;NO.3;PAGE.261-269(2000)
Figure&Table&Reference;FIG.6, TBL.1, REF.37
Pub. Country;Japan
Language;English
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 .BETA.-cells, we determined the expression of putative sphingosine 1-phosphate (S1P) receptors and the effect of sphingosine on pancreatic .BETA.-cell function using a clonal Hamster .BETA.-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 20 .MU.M S1P significantly stimulated insulin secretion for 10 minutes in HIT-T 15 cells. Ten .MU.M S1P significantly increased insulin secretion from isolated mouse islets. Ten .MU.M 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 .MU.M U73122 (phospholipase C inhibitor) completely deleted 10 .MU.M 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 100 ng/ml pertussis toxin (PTX) partially, but significantly attenuated an increase of insulin secretion by 10 .MU.M 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. (author abst.)
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