General Information:

Id: 2,977 (click here to show other Interactions for entry)
Diseases: Diabetes mellitus, type II - [OMIM]
Insulin resistance
MODY, type VI - [OMIM]
Mus musculus
neuroD beta-CKO mouse: mouse in which neuroD is deleted in insulin-expressing cells
Reference: Gu C et al.(2010) Pancreatic beta cells require NeuroD to achieve and maintain functional maturity Cell Metab 11: 298-310 [PMID: 20374962]

Interaction Information:

Comment Mutant mice in which neuroD is deleted in insulin-expressing cells (neuroD beta-CKO mice) and control mice had a similar amount of hepatic glucose-6-phosphatase (G6Pase) mRNA, an indicator of gluconeogenesis, when fasted overnight, suggesting that gluconeogenesis was equally stimulated in both cases. However, at 90 min after glucose injection, G6Pase mRNA fails to decrease in the mutant mice. Because insulin is a powerful inhibitor of G6Pase expression, the failure to downregulate G6Pase mRNA in neuroD beta-CKO mice is likely due to their severe insulin secretion defect. Therefore, in neuroD beta-CKO mice, sustained gluconeogenesis may exacerbate hyperglycemia during glucose challenge.
Formal Description
Interaction-ID: 27114



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