Deletion of nicotinamide nucleotide transhydrogenase: a new quantitive trait locus accounting for glucose intolerance in C57BL/6J mice.
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. C57B...
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Format: | Journal article |
Language: | English |
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2006
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author | Freeman, H Hugill, A Dear, N Ashcroft, F Cox, R |
author_facet | Freeman, H Hugill, A Dear, N Ashcroft, F Cox, R |
author_sort | Freeman, H |
collection | OXFORD |
description | 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. |
first_indexed | 2024-03-06T23:51:29Z |
format | Journal article |
id | oxford-uuid:72bfec7e-fe2c-4632-a0f4-9a1d63d58a23 |
institution | University of Oxford |
language | English |
last_indexed | 2024-03-06T23:51:29Z |
publishDate | 2006 |
record_format | dspace |
spelling | oxford-uuid:72bfec7e-fe2c-4632-a0f4-9a1d63d58a232022-03-26T19:52:08ZDeletion of nicotinamide nucleotide transhydrogenase: a new quantitive trait locus accounting for glucose intolerance in C57BL/6J mice.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:72bfec7e-fe2c-4632-a0f4-9a1d63d58a23EnglishSymplectic Elements at Oxford2006Freeman, HHugill, ADear, NAshcroft, FCox, RThe 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. |
spellingShingle | Freeman, H Hugill, A Dear, N Ashcroft, F Cox, R Deletion of nicotinamide nucleotide transhydrogenase: a new quantitive trait locus accounting for glucose intolerance in C57BL/6J mice. |
title | Deletion of nicotinamide nucleotide transhydrogenase: a new quantitive trait locus accounting for glucose intolerance in C57BL/6J mice. |
title_full | Deletion of nicotinamide nucleotide transhydrogenase: a new quantitive trait locus accounting for glucose intolerance in C57BL/6J mice. |
title_fullStr | Deletion of nicotinamide nucleotide transhydrogenase: a new quantitive trait locus accounting for glucose intolerance in C57BL/6J mice. |
title_full_unstemmed | Deletion of nicotinamide nucleotide transhydrogenase: a new quantitive trait locus accounting for glucose intolerance in C57BL/6J mice. |
title_short | Deletion of nicotinamide nucleotide transhydrogenase: a new quantitive trait locus accounting for glucose intolerance in C57BL/6J mice. |
title_sort | deletion of nicotinamide nucleotide transhydrogenase a new quantitive trait locus accounting for glucose intolerance in c57bl 6j mice |
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