What is the impact of the Nnt deletion in C57BL/6J mice?
The C57BL/6J male mouse has been the paradigm strain for studies of high fat diet-induced obesity (DIO). A recent report (see abstract below) indicates that this strain’s low insulin secretion in response to acute glucose challenge is attributable to a mutation in the NAD nucleotide transhydrogenase gene (Nnt, Chromosome 13). This finding raises the question as to whether this mutation is a major factor in the strain’s high sensitivity to DIO. This seems unlikely because C57BL/6N, which expresses a wildtype Nnt gene, reportedly is also DIO-sensitive. Moreover, males of certain other Nnt-intact strains, such as NON/ShiLtJ (formerly NON/LtJ), show even greater DIO responsiveness than do C57BL/6J males. The Jackson Laboratory currently has a study in progress to compare the DIO responsiveness of C57BL/6J and C57BL/6N males in the same vivarium. In a general sense, such deletions are often found as a result of intensively studying a mouse strain, especially a strain with a sequenced genome
