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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, we had previously performed quantitative trait locus (QTL) analysis, using (SM/J×SMXA-5)F2 intercross mice, and identified  Fl1sa  on chromosome 12 (centromere-53.06 Mb) as a significant QTL for fatty liver. Furthermore, 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-12 SM  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, we created  Iah1  knockout (KO) mice with two different backgrounds [C57BL/6N (B6) and A/J-12 SM  (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 hands, 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, we 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 .

Ablation of Iah1, a candidate gene for diet-induced fatty liver, does not affect liver lipid accumulation in mice