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Literature summary for 1.4.1.2 extracted from

  • Carobbio, S.; Frigerio, F.; Rubi, B.; Vetterli, L.; Bloksgaard, M.; Gjinovci, A.; Pournourmohammadi, S.; Herrera, P.L.; Reith, W.; Mandrup, S.; Maechler, P.
    Deletion of glutamate dehydrogenase in beta-cells abolishes part of the insulin secretory response not required for glucose homeostasis (2009), J. Biol. Chem., 284, 921-929.
    View publication on PubMed
Search for more literature for 1.4.1.2

Application

Application Comment Organism
molecular biology GDH is essential for the full development of the secretory response in beta-cells Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
mitochondrion
-
 Mus musculus 5739
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Organism

Organism UniProt Comment Textmining
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
pancreatic beta cell
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 Mus musculus
-

Synonyms

Synonyms Comment Organism
glutamate dehydrogenase
-
 Mus musculus

General Information

General Information Comment Organism
physiological function transgenic mice, betaGlud1-/-, are generated bearing a beta-cell-specific GDH deletion. In situ pancreatic perfusion reveals that glucose-stimulated insulin secretion is reduced by 37% in transgenic mice. Isolated islets with either constitutive or acute adenovirus-mediated knock-out of GDH show a 49 and 38% reduction in glucose-induced insulin release, respectively. Adenovirus-mediated re-expression of GDH in transgenic mice fully restores glucose-induced insulin release. In transgenic mice reduced secretory capacity results in lower plasma insulin levels in response to both feeding and glucose load, while body weight gain is preserved Mus musculus