Sphingosine-1-phosphate　(S1P)　has　been　reported　to　enhance　the　function　of　islet　beta-cells,　providing　a　potential　therapeutic　target　for　diabetes　mellitus.　In　the　present　study,　the　effects　of　S1P　on　the　proliferation　and　apoptosis　of　beta-cells　in　type　2　diabetic　mice　were　investigated.　The　mice　were　administered　intraperitoneal　S1P　solution　daily　at　a　dose　of　20　mu　g/kg　for　three　weeks.　The　intraperitoneal　glucose　tolerance　test　(IPGTT)　and　homeostatic　model　assessment　of　insulin　resistance　(HOMA-IR)　index　determination　were　carried　out.　Immunohistochemical　staining　was　used　to　detect　the　protein　expression　of　insulin,　antigen　Ki-67　and　S1P　receptor　isoforms　(S1PR1/S1PR2/S1PR3)　in　pancreatic　islets.　Compared　with　the　diabetic　control　(DC)　group,　the　IPGTT　results　and　HOMA-IR　index　in　the　S1P　treatment　group　were　decreased.　The　islets　in　the　S1P　group　exhibited　higher　insulin　immunostaining　intensity　than　the　DC　group,　as　well　as　higher　proliferation　(P＜0.05)　and　lower　apoptosis　rates　(P＜0.05).　Positive　staining　for　the　S1P　receptors　S1PR1,　S1PR2　and　S1PR3　was　observed　in　the　cytoplasm　and　membrane　of　the　islet　cells.　S1PR1　and　S1PR2　proteins　showed　increased　expression　in　the　S1P　and　DC　groups　compared　with　the　normal　control　group　(P＜0.01　and　P＜0.05,　respectively),　whereas　no　significant　difference　was　observed　in　the　expression　of　S1PR3　among　these　groups.　In　conclusion,　extracellular　S1P　can　induce　islet　beta-cell　proliferation　and　decrease　cell　apoptosis　in　diabetic　mice.　S1P　function　may　be　mediated　via　S1PR1　and　S1PR2;　therefore,　targeting　S1P/S1PR　signalling　pathways　may　be　a　novel　therapeutic　strategy　for　diabetes　mellitus.