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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Ppargtm2Avp
targeted mutation 2, Antonio Vidal-Puig
MGI:3711168
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Ppargtm2Avp/Ppargtm2Avp involves: 129/Sv * C57BL/6 MGI:3711741
hm2
Ppargtm2Avp/Ppargtm2Avp Not Specified MGI:3711710
cx3
Lepob/Lepob
Ppargtm2Avp/Ppargtm2Avp
involves: 129 * C57BL/6 MGI:3711740


Genotype
MGI:3711741
hm1
Allelic
Composition
Ppargtm2Avp/Ppargtm2Avp
Genetic
Background
involves: 129/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppargtm2Avp mutation (0 available); any Pparg mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• short chain triacylglycerides in islets are decreased

homeostasis/metabolism




Genotype
MGI:3711710
hm2
Allelic
Composition
Ppargtm2Avp/Ppargtm2Avp
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppargtm2Avp mutation (0 available); any Pparg mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
N
• mice breed normally

homeostasis/metabolism
• despite reduction of adiponectin levels plasma leptin levels are increased on a normal and high fat diet
• when fed a normal diet, mice show decreased insulin-increased glucose turnover, glucose turnover rates and whole body glucose synthesis
• fasted glucose levels are increased in the presence of increased plasma insulin
• at 16 weeks of age, male but not female mice exhibit glucose intolerance when fed a normal or high fat diet
• levels are reduced under a normal diet but levels fail to reduce further under a high fat diet (HFD) regime

adipose tissue
• intradermal fat deposits are reduced at 16 and 32 weeks
• although adipose tissue differentiates properly in vivo, preadipocytes differentiate poorly in vitro
• preferential deposition of fat subcutaneously without reduction in the intra-abdominal/peridonadal fat pad on a normal and high fat diet
• after being fed a high fat diet (HFD), mice exhibit adipocyte hypertrophy
• while fewer long-chain triacylglycerols species and C32:n phosphatidylcholines are produced, there is an upregulation of a cluster of lipids containing short-chain triacylglycerols, long-chain phospholipids, lyso-phoslipids, diacylclycerols and ceramide-related compounds
• however, total lipid content is the same as in wild-type mice




Genotype
MGI:3711740
cx3
Allelic
Composition
Lepob/Lepob
Ppargtm2Avp/Ppargtm2Avp
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lepob mutation (5 available); any Lep mutation (21 available)
Ppargtm2Avp mutation (0 available); any Pparg mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• although female mice consume a similar amount of oxygen as Lepob homozygotes, double homozygous females have a lower respiratory exchange ratio in a fed state
• however, no difference in the respiratory exchange ratio is seen in the fasted state compared Lep single homozygotes
• insulin secretion is impaired compared to Lepob homozygotes under basal and stimulated condition even when corrected for insulin content
• develops earlier than in than Lepob homozygotes at 4 weeks
• however, no differences in glucose levels are found at 3 to 5 days after birth
• develops at 4 weeks of age in conjunction with a change to chow feed
• at 16 weeks, males have severe hyperglycemia in fed and fasted states whereas females have a milder phenotype
• at 16 weeks male mice, and to a lesser extend female mice, have inappropriately low insulin levels
• plasma insulin levels are lower than in Lepob homozygotes
• at 4 weeks insulin levels are increased to a similar extent as in Lepob homozygotes
• at 16 weeks in male mice, and to a lesser extent in female mice, insulin levels are elevated relative to wild-type mice but reduced levels relative to Lepob homozygotes
• insulin resistance is more severe and develops earlier (by 4 weeks of age) than in Lepob homozygotes
• decrease in triacylglycerides and accumulation of reactive lipid species in adipose tissue, pancreatic islets, liver, and skeletal muscle
• decrease in short and medium chain triacylglyceride levels

endocrine/exocrine glands
N
• despite insulin resistance, beta cell mass is similar to wild-type mice
• at 16 weeks, islet cells are decreased in number and size (30% smaller) and insulin content is 30-fold lower compared to Lepob homozygotes
• at 16 weeks, islets from females are grey, have irregular surfaces and require less time for collagenase digestion
• decrease in short chain triacylglyceride levels and increase in concentrations of reactive lipid species
• at 4 weeks of age no differences in pancreas morphology are seen
• alpha cells are scattered rather than forming a rim around the beta cells
• insulin secretion is impaired compared to Lepob homozygotes under basal and stimulated condition even when corrected for insulin content

behavior/neurological
• water consumption is significantly increased at 6 weeks of age compared to Lepob homozygotes
• mice are hyperphagic
• at 6 weeks, night activity is increased compared to Lepob homozygotes
• at 20 weeks, mice are less active compared to wild-type mice or Ppargtm1Avb homozygotes
• however, activity levels are comparable to those seen in Lepob homozygotes

adipose tissue
• at 16 weeks, mice have fewer small adipocytes compared to Lepob homozygotes or wild-type mice
• at 20 weeks, mice have a 4% increase body fat composition compared to wild-type mice, which is less than the 40% increase in Lepob homozygotes

growth/size/body
N
• over a 12 week period, mice maintain a normal weight unlike Lepob homozygotes

liver/biliary system
• increase in levels of reactive lipid species
• decrease in short and medium chain triacylglyceride levels
• increase in hepatic fat deposition compared to wild-type and Ppargtm1Avb homozygotes but not as severe as in Lepob homozygotes

muscle
• decrease in triacylglyceride levels and increase in reactive lipid species levels

renal/urinary system

cellular
• increased compared to Lepob homozygotes





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory