Mapping Data

Experiment

• Experiment
  TEXT-QTL-Candidate Genes
• Chromosome
  12
• Reference
  J:289414 Masuya T, et al., Ablation of Iah1, a candidate gene for diet-induced fatty liver, does not affect liver lipid accumulation in mice. PLoS One. 2020;15(5):e0233087
• ID
  MGI:6487874

Genes

Gene	Assay Type
Fl1sa	visible phenotype
Iah1	visible phenotype

Notes

• Experiment
  Nonalcoholic fatty liver disease (NAFLD) is a pathological condition caused by excess triglyceride deposition in the liver. The SMXA-5 severe fatty liver mouse model has been established from the SM/J and A/J strains. To explore the genetic factors involved in fatty liver development in SMXA-5 mice, the authors had previously performed QTL analysis, using (SM/JSMXA-5)F2 intercross mice, and identified Fl1sa on Chromosome 12 (centromere-53.06 Mb) as a significant QTL for fatty liver.
  
  Isoamyl acetate-hydrolyzing esterase 1 homolog (Iah1) was selected as the most likely candidate gene for Fl1sa. Iah1 gene expression in fatty liver-resistant A/J-12SM mice was significantly higher than in fatty liver-susceptible A/J mice. These data indicated that the Iah1 gene might be associated with fatty liver development. However, the function of murine Iah1 remains unknown.
  
  Therefore, in this study, the authors created Iah1 knockout (KO) mice with two different backgrounds [C57BL/6N (B6) and A/J-12SM (A12)] to investigate the relationship between Iah1 and liver lipid accumulation. Liver triglyceride accumulation in Iah1-KO mice of B6 or A12 background did not differ from their respective Iah1-wild type mice under a high-fat diet. These results indicated that loss of Iah1 did not contribute to fatty liver.
  
  On the other hand, adipose tissue dysfunction causes lipid accumulation in ectopic tissues (liver, skeletal muscle, and pancreas). To investigate the effect of Iah1 deficiency on white adipose tissue, the authors performed DNA microarray analysis of epididymal fat in Iah1-KO mice of A12 background. This result showed that Iah1 deficiency might decrease adipokines Sfrp4 and Metrnl gene expression in epididymal fat.
  
  This study demonstrated that Iah1 deficiency did not cause liver lipid accumulation and that Iah1 was not a suitable candidate gene for Fl1sa.