Mouse Genome Informatics
hm1
    Acox1tm1Jkr/Acox1tm1Jkr
involves: 129P2/OlaHsd * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype

Hepatocellular alterations in liver of Acox1tm1Jkr/Acox1tm1Jkr mice

tumorigenesis
• hepatic adenomas and carcinomas developed by 15 months of age, putatively due to sustained activation of Ppara
• hepatic adenomas and carcinomas developed by 15 months of age, putatively due to sustained activation of Ppara

liver/biliary system
• liver weight accounted for ~11% of total body weight compared to 4% in wild-type mice
• severe microvesicular fatty metamorphosis
• impaired peroxisome assembly, hepatocyte cell death followed by hepatocellular regeneration
• regenerated hepatocytes exhibited massive spontaneous peroxisome proliferation and led to a complete reversal of fatty metamorphosis by 6 to 8 months of age

homeostasis/metabolism
• accumulation of very long chain fatty acids in blood

reproductive system
(J:35794)
(J:35794)
• reduced numbers of spermatozoa (J:35794)
• reduced numbers of round spermatids (J:35794)
(J:35794)

growth/size/body
• mutant mice weighed 40 to 50% less than wild-type littermates during first 5 months of age

endocrine/exocrine glands
(J:35794)
(J:35794)

Mouse Models of Human Disease
OMIM IDRef(s)
Peroxisomal Acyl-Coa Oxidase Deficiency 264470 J:35794


Mouse Genome Informatics
ht2
    Acox1tm1Jkr/Acox1+
involves: 129P2/OlaHsd * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
liver/biliary system
• mild microvesicular fatty metamorphosis