JAX Notes October 01, 2006

Cause of impaired glucose tolerance in C57BL/6J mice discovered

In 2006, by performing QTL analysis in an intercross between C57BL/6J (000664) strain, a widely used model of diet-induced diabetes, and C3H/HeJ (000659), researchers from the United Kingdom recently found strong evidence that a spontaneous in-frame five-exon deletion in the nicotinamide nucleotide transhydrogenase (Nnt) gene is partly responsible for impaired glucose tolerance and reduced insulin secretion in C57BL/6J mice. C57BL/6J mice transgenic for the entire Nnt gene had normal phenotypes. This discovery may offer insight into the poorly understood genetic reasons for aberrant glucose homeostasis in type 2 diabetes.

Reference

Freeman HD, Hugill A, Dear NT, Ashcroft FM, Cox RD. 2006. Deletion of nicotinamide nucleotide transhydrogenase: a new quantitative trait locus accounting for glucose intolerance in C57BL/6J mice. Diabetes 55:2153-6