Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  10
• Reference
  J:80998 Kobayashi M, et al., Combinations of nondiabetic parental genomes elicit impaired glucose tolerance in mouse SMXA recombinant inbred strains. Diabetes. 2003 Jan;52(1):180-6
• ID
  MGI:2675242

Genes

Gene	Assay Type
T2dm1sa	visible phenotype
D10Mit136	PCR amplified length variant
Kcnc2	reported elsewhere

Notes

• Experiment
  19 SMXA RI strains were analyzed for 789 polymorphic markers at an average resolution of 4 cM to identify QTLs associated with impaired glucose tolerance. Animals were placed on a high-carbohydrate diet for 11 weeks. Parental strain A/J exhibits a higherbody mass index (BMI) and increased blood glucose concentration at 120 minutes during the intraperitoneal glucose tolerance test (IPTGG) compared to parental strain SM/J.
  
  A locus reaching statistical significance for nonfasting glucose concentration mapped to 62 cM on mouse Chromosome 10 with LOD=3.8 at D10Mit136 and is called Nfbg. This locus is also suggestively linked to IPGTT at 120 minutes with LOD=2.6. SM/J-derived alleles appear to confer increased blood glucose concentrations at Nfbg. A possiblecandidate gene for Nfbg is Kcnc2.
  
  Several suggestive linkages were also detected on mouse Chromosome 2 for IPTGG at 30 minutes (LOD=2.0 at D2Mit6 with A/J-derived alleles conferring increased blood glucose concentrations), mouse Chromosome 6 for BMI (LOD=3.2 at D6Mit17) and nonfasting blood glucose concentrations (LOD=2.3 at D6Mit287 with A/J-derived alleles conferring increased blood glucose concentrations), and mouse Chromosome 18 for nonfasting blood glucose concentrations (LOD=2.5 at D18Mit20) and fasting blood glucose concentrations (LOD=2.0 at D18Mit17). A/J-derived alleles confer increased blood glucose concentrations at both chromosome 18 loci.