Mice homozygous for the fat spontaneous mutation (Cpefat) become noticeably obese by 14-15 weeks of age. Homozygous mutant mice develop a diabetic phenotype characterized by hyperglycemia and insulin resistance.Read More +
Mice homozygous for the fat spontaneous mutation (Cpefat) on a C57BL/6J genetic background (N10) become noticeably obese by 14-15 weeks of age. There is also some sexual dimorphism; female homozygous mutant mice develop obesity at a later age than males. Cpefat mice actually weigh less than wildtype controls prior to weaning age. Homozygous mutant mice develop a diabetic phenotype characterized by hyperglycemia and insulin resistance. Cpefat mice appear healthier on the C57BL/6J genetic background, avoiding the hereditary hydronephrosis present in C57BLKS/J and a lower incidence of malocclusion.
The Cpefat mutation arose on HRS/J (Hummel et al., 1974).
|Gene Symbol and Name||Cpe, carboxypeptidase E|
|Strain of Origin||HRS/J|
|Molecular Note||The molecular mutation responsible for the phenotype in the fat mouse is a T to C transition at coding nucleotide 730 of the mRNA. The codon of this nucleotide corresponds to amino acid 244 of the unprocessed preproenzyme or amino acid 202 of the mature peptidase. The mutation alters a conserved serine to a proline residue in the encoded protein (p.S244P). Enzymatic activity of the mutant protein was shown to be abolished in fluorometric assays in vitro.|
When using the B6.HRS(BKS)-Cpefat/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #003923 in your Materials and Methods section.