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Phenotypes Associated with This Genotype
Genotype
MGI:3818949
Allelic
Composition
Ppargtm1Tka/Pparg+
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppargtm1Tka mutation (0 available); any Pparg mutation (39 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die after the 37th week following treatment with MNU due to gastric tumors

homeostasis/metabolism
• when fed a high fat diet, mice do not gain as much weight as similarly treated wild-type mice
• however, when fed a high carbohydrate diet mice gain as much weight as wild-type mice and treatment with pioglitazone restores high fat diet-induced obesity
• when fed a high fat diet compared to similarly treated wild-type mice
• however, treatment with pioglitazone increases insulin levels when mice are fed a high fat diet
• when fed a high fat diet, leptin serum levels are 1.8-fold higher than in similarly treated wild-type mice
• when fed a high fat diet
• when fed a high fat diet, mice exhibit insulin sensitivity instead of insulin resistance as do similarly treated wild-type mice
• however, treatment with pioglitazone decreases insulin sensitivity when mice are fed a high fat diet
• mice die after the 37th week following treatment with MNU due to gastric tumors
• following treatment with MNU, mice develop gastric cancer (in 17 of 19 mice) of with 1 is a carcinoma in, 15 are well-differentiated adenocarcinomas, 1 is a moderately differentiated adenocarcinoma and 1 is a lymphoma compared to similarly treated wild type mice that develop gastric carcinoma (in 5 of 9 mice) all of which are well-differentiated adenocarcinomas
• unlike in wild-type mice, treatment with troglitazone does no inhibit MNU-induced carcinogenesis
• following pressure overload, mice exhibit increased cardiac hypertrophy and increased interventricular septum and left ventricular posterior wall thickness compared to in similarly treated wild-type mice
• however, treatment of pressure overloaded mice with pioglitazone reduces cardiac hypertrophy

skeleton
N
• despite increased osteoblast number and bone formation, osteoclast physiology is normal and mice exhibit normal bone loss following ovariectomy
• osteoblastgenesis is increased compared to in wild-type mice
• in vitro, osteoblastgenesis from bone marrow progenitors is increased compared to in wild-type mice
• however, calvarial osteoblasts, which are more mature than bone marrow cells, exhibit normal morphology and physiology
• at 8 weeks and 52 weeks of age, the number of adipocytes within the bone marrow is lower than in wild-type mice
• the numbers of osteoblast surface and osteoid surface are doubled compared to in wild-type mice
• at 8 weeks and 52 weeks of age, trabecular bone mass is increased 40% compared to in wild-type mice
• bone formations is twice as much as in wild-type mice due to increased numbers of osteoblasts

adipose tissue
• when fed a high fat diet, brown adipose tissue mass is decreased 40% compared to in similarly treated wild-type mice
• when fed a high fat diet, mice exhibit a more than 70% inhibition in the increase in white adipose tissue mass observed similarly treated wild-type mice
• however, treatment with pioglitazone results in increased adipose tissue when fed a high fat diet
• when fed a high fat diet, adipocyte size is less than in similarly treated wild-type mice (J:58222)
• when fed a high fat diet, brown adipose tissue adipocytes are 36% smaller than in similarly treated wild-type mice (J:58222)
• however, treatment with pioglitazone increases adipocyte size when mice are fed a high fat diet (J:58222)
• at 8 weeks and 52 weeks of age, the number of adipocytes within the bone marrow is lower than in wild-type mice (J:89250)

cellular
• 50% fewer embryonic fibroblasts differentiate into adipose cells compared to wild-type embryonic fibroblast cells
• however, pioglitazone partially rescued adipocyte differentiation
• osteoblastgenesis is increased compared to in wild-type mice
• in vitro, osteoblastgenesis from bone marrow progenitors is increased compared to in wild-type mice
• however, calvarial osteoblasts, which are more mature than bone marrow cells, exhibit normal morphology and physiology

behavior/neurological
• when fed a high fat diet

growth/size/body
• when fed a high fat diet, mice do not gain as much weight as similarly treated wild-type mice
• however, when fed a high carbohydrate diet mice gain as much weight as wild-type mice and treatment with pioglitazone restores high fat diet-induced obesity

liver/biliary system

neoplasm
• following treatment with MNU, mice develop gastric cancer (in 17 of 19 mice) of with 1 is a carcinoma in, 15 are well-differentiated adenocarcinomas, 1 is a moderately differentiated adenocarcinoma and 1 is a lymphoma compared to similarly treated wild type mice that develop gastric carcinoma (in 5 of 9 mice) all of which are well-differentiated adenocarcinomas
• unlike in wild-type mice, treatment with troglitazone does no inhibit MNU-induced carcinogenesis

cardiovascular system
• following treatment with STZ, mice exhibit a 2.1-fold increase in retinal leukostasis compared to in similarly treated wild-type mice
• following treatment with STZ, retinal leakage is increased 1.9-fold compared to in similarly treated wild-type mice

immune system
• following treatment with STZ, mice exhibit a 2.1-fold increase in retinal leukostasis compared to in similarly treated wild-type mice
• cultured bone marrow cells exhibit reduced adipogenesis but increased osteogenesis compared to wild-type cells

vision/eye
• following treatment with STZ, mice exhibit a 2.1-fold increase in retinal leukostasis compared to in similarly treated wild-type mice
• following treatment with STZ, retinal leakage is increased 1.9-fold compared to in similarly treated wild-type mice

hematopoietic system
• following treatment with STZ, mice exhibit a 2.1-fold increase in retinal leukostasis compared to in similarly treated wild-type mice


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
04/30/2024
MGI 6.23
The Jackson Laboratory