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Caption | Constitutive Beta-cell specific Glud1 knock-out impairs insulin secretion that is rescued by GDH ectopic re-expression. A) After an overnight culture, islets isolated from the two groups were hand-picked and distributed into perifusion chambers. Insulin release was measured in the effluent of chambers perifused first with basal 2.8 mM glucose before stimulation for 20 min with 22.8 mM glucose. Compared with controls, islets isolated from Glud1tm1.1Pma/Glud1tm1.1Pma Tg(Ins2-cre)23Herr/0 (betaGlud1-/-) mice exhibited marked reduction of the secretory responses during first phase (-68%, p<0.01) and second sustained phase (-49%, p<0.05), n = 7. B) Islets isolated from Glud1tm1.1Pma/Glud1tm1.1Pma Tg(Ins2-cre)23Herr/0 mice were transduced with adenovirus AdGDH carrying hGLUD1 to restore GDH expression. Insulin secretion was measured over a 15-min period at basal 2.8 mM (Glc 2.8) and stimulatory 22.8 mM glucose (Glc 22.8) on batches of 10 islets, *, p<0.05 versus control Glc 22.8; S, p<0.05 versus corresponding group at Glc 2.8 (n = 3). | ||||
Copyright | This image is from Carobbio S, J Biol Chem 2009 Jan 9;284(2):921-9 and is displayed with the permission of the American Society for Biochemistry and Molecular Biology who owns the Copyright. Full text from JBC. J:145558 | ||||
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 11/12/2024 MGI 6.24 |
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