![]() If you want to use this software on your smartphone, just download it, install it and open the mobile app, select your smartphone from the devices list, then you are all set. As a result of this limitation, the majority of people use the Remote Mouse on their smartphones, which is not a bad thing since most people these days use more than one smartphone simultaneously. ![]() You are not able to use it if you have more than one smartphone. The free version of the Remote Mouse allows connecting only one smartphone at a time. Using the Bluetooth technology, Remote Mouse can synchronize with your Windows Mobile Mouse without any extra hardware. Just install both apps and then you will easily be controlling your computer with your mobile device effortlessly. You can either do it with the Remote Mouse or with the special Windows Mobile Mouse. Connect your laptop/tablet to the Internet using the Bluetooth technology. Published by Elsevier Inc.Remote Mouse is also available for iPhone/iPad, iPad, Android and Windows Phones with a Bluetooth companion app for Mac and Windows. The promoting effects of dapagliflozin on beta cell regeneration may be partially mediated via GLP-1 secreted from alpha cells. Dapagliflozin enhances beta cell self-replication, induces alpha to beta cell conversion, and promotes duct-derived beta cell neogenesis. Conclusions: Except for glucose-lowering effect, dapagliflozin has extra protective effects on beta cells in type 2 diabetes. Importantly, the dapagliflozin-induced upregulation of Pdx1 expression was attenuated by GLP-1 receptor antagonist. Moreover, dapagliflozin upregulated the expression of Pcsk1 (which encodes prohormone convertase 1/3, an important enzyme for processing proglucagon to GLP-1), and increased GLP-1 content and secretion in alpha TC1.9 cells. In cultured primary rodent islets and alpha TC1.9 cells, dapagliflozin upregulated the expression of pancreatic endocrine progenitor and beta cell specific markers (including Pdx1) under high glucose condition. After the dapagliflozin treatment, some insulin-positive cells were located in the duct compartment or even co-localized with duct cell markers, suggestive of duct-derived beta cell neogenesis. The alpha to beta cell conversion, as evaluated by glucagon and insulin double-positive cells and confirmed by using alpha cell lineage-tracing, was facilitated by dapagliflozin. The beta cell proliferation as indicated by C-peptide and BrdU double-positive cells was boosted by dapagliflozin. The dapagliflozin treatment increased islet and beta cell numbers in the two diabetic mice. Results: Treatment with dapagliflozin significantly decreased blood glucose in the two diabetic models and upregulated plasma insulin and GLP-1 levels in db/db mice. The expression of specific markers and hormone levels were determined. ![]() Primary rodent islets and alpha TC1.9, a mouse alpha cell line, were incubated with dapagliflozin (0.25-25 mu mol/L) or vehicle in the presence or absence of GLP-1 receptor antagonist for 24 h in regular or high glucose medium. The evaluation of islet morphology and cell phenotype was performed with immunofluorescence. The plasma insulin, glucagon and glucagon-like peptide-1 (GLP-1) were determined by using ELISA. Mice were treated by daily intragastric administration of dapagliflozin (1 mg/kg) or vehicle for 6 weeks. Methods: Two diabetic mouse models, db/db mice and pancreatic alpha cell lineage-tracing (glucagon-beta-gal) mice whose diabetes was induced by high fat diet combined with streptozotocin, were used. Our study aimed to investigate the effect of dapagliflozin on islet morphology and cell phenotype, and explore the origin and possible reason of the regenerated beta cells. Peking Univ Third Hosp, Clin Stem Cell Res Ctr, Beijing 100191, Peoples R Chinaīackground: Clinical trials and animal studies have shown that sodium-glucose co-transporter type 2 (SGLT2) inhibitors improve pancreatic beta cell function. Peking Univ Third Hosp, Dept Endocrinol & Metab, Beijing 100191, Peoples R China Dapagliflozin promotes beta cell regeneration by inducing pancreatic endocrine cell phenotype conversion in type 2 diabetic mice
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