| First Author | Freeman HC | Year | 2006 |
| Journal | Diabetes | Volume | 55 |
| Issue | 7 | Pages | 2153-6 |
| PubMed ID | 16804088 | Mgi Jnum | J:109356 |
| Mgi Id | MGI:3628796 | Doi | 10.2337/db06-0358 |
| Citation | Freeman HC, et al. (2006) Deletion of Nicotinamide Nucleotide Transhydrogenase: A New Quantitive Trait Locus Accounting for Glucose Intolerance in C57BL/6J Mice. Diabetes 55(7):2153-6 |
| abstractText | The C57BL/6J mouse displays glucose intolerance and reduced insulin secretion. The genetic locus underlying this phenotype was mapped to nicotinamide nucleotide transhydrogenase (Nnt) on mouse chromosome 13, a nuclear-encoded mitochondrial protein involved in beta-cell mitochondrial metabolism. C57BL/6J mice have a naturally occurring in-frame five-exon deletion in Nnt that removes exons 7-11. This results in a complete absence of Nnt protein in these mice. We show that transgenic expression of the entire Nnt gene in C57BL/6J mice rescues their impaired insulin secretion and glucose-intolerant phenotype. This study provides direct evidence that Nnt deficiency results in defective insulin secretion and inappropriate glucose homeostasis in male C57BL/6J mice. |
