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      Deletion of nicotinamide nucleotide transhydrogenase: a new quantitive trait locus accounting for glucose intolerance in C57BL/6J mice.

      Diabetes

      Animals, Blood Glucose, metabolism, Chromosomes, Artificial, Bacterial, Exons, Glucose Intolerance, enzymology, genetics, Insulin, blood, Mice, Mice, Inbred C3H, Mice, Inbred C57BL, Mice, Transgenic, NADP Transhydrogenases, deficiency, Quantitative Trait Loci, Sequence Deletion

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          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 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.

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          Journal
          16804088
          10.2337/db06-0358

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