Abstract
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 β-cell mitochondrial metabolism. C57BL/6J mice have a naturally occurring inframe 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.
Original language | English |
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Pages (from-to) | 2153-2156 |
Number of pages | 4 |
Journal | Diabetes |
Volume | 55 |
Issue number | 7 |
DOIs | |
Publication status | Published - 1 Jul 2006 |
Keywords
- BAC, bacterial artificial chromosome
- IPGTT, intraperitoneal glucose tolerance test
- Nnt, nicotinamide nucleotide transhydrogenase
- QTLs, quantitative trait loci
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism