Analysis Tools
cellular
 |
• reduced numbers of round spermatids
|
neoplasm
|
• hepatic adenomas and carcinomas developed by 15 months of age, putatively due to sustained activation of Ppara
|
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• 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
|
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• severe microvesicular fatty metamorphosis
|
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• hepatic adenomas and carcinomas developed by 15 months of age, putatively due to sustained activation of Ppara
|
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• 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
|
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• regenerated hepatocytes exhibited massive spontaneous peroxisome proliferation and led to a complete reversal of fatty metamorphosis by 6 to 8 months of age
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homeostasis/metabolism
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• accumulation of very long chain fatty acids in blood
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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 | |
