期刊
DIABETES
卷 55, 期 7, 页码 2153-2156出版社
AMER DIABETES ASSOC
DOI: 10.2337/db06-0358
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资金
- Medical Research Council [MC_U142661184, MC_U142684172, MC_U142684175, MC_UP_1502/1] Funding Source: researchfish
- MRC [MC_U142684175, MC_U142661184, MC_U142684172, MC_UP_1502/1] Funding Source: UKRI
- Medical Research Council [MC_U142684175, MC_U142684172, MC_UP_1502/1, MC_U142661184] Funding Source: Medline
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 Nut 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 Nut deficiency results in defective insulin secretion and inappropriate glucose homeostasis in male
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