cellular
• reduced numbers of round spermatids
|
neoplasm
• 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
|
• 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
|
pale liver
(
J:35794
)
• 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
small ovary
(
J:35794
)
|
small testis
(
J:35794
)
|
• reduced numbers of spermatozoa
|
• reduced numbers of round spermatids
|
growth/size/body
• mutant mice weighed 40 to 50% less than wild-type littermates during first 5 months of age
|
• liver weight accounted for ~11% of total body weight compared to 4% in wild-type mice
|
endocrine/exocrine glands
small ovary
(
J:35794
)
|
small testis
(
J:35794
)
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
peroxisomal acyl-CoA oxidase deficiency | DOID:0050797 |
OMIM:264470 |
J:35794 |