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Mice homozygous for the targeted mutation are viable and
fertile. An altered response to a group of compounds
(peroxisome proliferators) that induce peroxisome
proliferation and hepatocarcinogenesis is observed. No
peroxisome proliferation response is detected when these
mice are challenged with classical peroxisome proliferators.
Typically, such a response includes hepatomegaly, peroxisome
proliferation and transcriptional activation of a set of
target enzyme genes. Accumulation of lipid droplets observed
in liver tissue suggests that Ppara is involved in
maintaining the homeostasis of hepatic lipid metabolism.
Homozygotes exhibit increased gonadal adipose tissue stores,
abnormal epidermal development and delayed wound healing.
This mutant mouse strain may be useful in studies of lipid
metabolism, cell proliferation, diabetes, obesity, and wound
increased gonadal fat pad weight; abnormal circulating
glucose level, abnormal circulating insulin level, increased
circulating triglyceride level; hepatic steatosis
Genomics - Modifications
Curation Flag Information
New comment to be added:
Ppar/Sable/GTT Order #7840 6/10/13
Vsg / sham in Ppar alpha deficient males / NIU063111
Vsg / sham in Ppar alpha deficient males / NIU063114
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Financial support for this work was provided by the NIDDK Mouse Metabolic Phenotyping Centers (National MMPC, RRID:SCR_008997,
) under the MICROMouse Program, grants DK076169.
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