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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Fabp4-cre)1Abel
transgene insertion 1, E Dale Abel
MGI:2182103
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Ptentm1Hwu/Ptentm1Hwu
Tg(Fabp4-cre)1Abel/0
involves: 129S4/SvJae MGI:4830361
cn2
Slc2a4tm1Abel/Slc2a4tm1Abel
Tg(Fabp4-cre)1Abel/?
involves: 129S4/SvJae * FVB MGI:3029364
cn3
Igf1rtm1Jcbr/Igf1rtm1Jcbr
Tg(Fabp4-cre)1Abel/?
involves: C57BL/6 * FVB/N MGI:3818455
cn4
Gnastm5.1Lsw/Gnastm5.1Lsw
Tg(Fabp4-cre)1Abel/0
involves: FVB MGI:6102945


Genotype
MGI:4830361
cn1
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
Tg(Fabp4-cre)1Abel/0
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Hwu mutation (16 available); any Pten mutation (83 available)
Tg(Fabp4-cre)1Abel mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
N
• no differences in body weight and fat storage

homeostasis/metabolism
• fasting mutants exhibit a 2.1-fold decrease in plasma insulin levels compared to controls indicating enhanced insulin sensitivity
• during a glucose tolerance test, mutants show a blunted elevation of blood glucose; the mean peak increase in blood glucose is 19% lower than that of controls
• mutants are protected from developing streptozotocin-induced diabetes; they maintain normal glycemia and remain resistant to the development of hyperglycemia
• mutants are more sensitive to insulin challenge (in insulin tolerance test), showing a 24% lower blood glucose at 60 min compared to wild-type mice
• insulin resistance is 1.9-fold lower for mutants than controls
• 36% lower serum concentrations of the adipocytokine resistin

immune system
• 36% lower serum concentrations of the adipocytokine resistin




Genotype
MGI:3029364
cn2
Allelic
Composition
Slc2a4tm1Abel/Slc2a4tm1Abel
Tg(Fabp4-cre)1Abel/?
Genetic
Background
involves: 129S4/SvJae * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc2a4tm1Abel mutation (0 available); any Slc2a4 mutation (35 available)
Tg(Fabp4-cre)1Abel mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• basal glucose uptake reduced about 40% in adipocytes
• insulin mediated glucose uptake was blunted to a maximum of about 72%
• whole body glucose uptake reduced 53%
• glycolysis down 50%
• transport in to white and brown adipose tissue and skeletal muscle reduced
• insulin unable to suppress hepatic glucose production
• impaired glucose tolerance as early as 13 weeks and persisting until after 31 weeks of age
• glycogen synthesis down 67%
• as early as 12 weeks and sometimes becomes extreme




Genotype
MGI:3818455
cn3
Allelic
Composition
Igf1rtm1Jcbr/Igf1rtm1Jcbr
Tg(Fabp4-cre)1Abel/?
Genetic
Background
involves: C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Igf1rtm1Jcbr mutation (0 available); any Igf1r mutation (85 available)
Tg(Fabp4-cre)1Abel mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• disproportionately increased at 24 weeks
• both males and females have gained more weight than controls by 10 weeks of age
• daily food intake normal
• significantly increased naso-anal length by 24-32 weeks of age
• disproportionately increased at 24 weeks

adipose tissue
• disproportionately increased in weight at 24 weeks
• increased number and diameter of adipocytes
• adipocyte abnormalities particularly evident in epigonadal fat

liver/biliary system
• disproportionately increased at 24 weeks

cardiovascular system
• disproportionately increased at 24 weeks

nervous system
• relative brain weight is significantly reduced at 24 weeks

homeostasis/metabolism
• fasted blood glucose significantly increased at 12 weeks but not 24 weeks of age
• fed blood glucose levels in males also increased at 12 weeks
• of isolated adipocytes
• significantly lower at 12 weeks




Genotype
MGI:6102945
cn4
Allelic
Composition
Gnastm5.1Lsw/Gnastm5.1Lsw
Tg(Fabp4-cre)1Abel/0
Genetic
Background
involves: FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gnastm5.1Lsw mutation (1 available); any Gnas mutation (53 available)
Tg(Fabp4-cre)1Abel mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle

mortality/aging
• by 14 weeks in severely affected mice

homeostasis/metabolism
N
• surviving mice exhibit normal food intake, energy expenditure and respiratory ratio at ambient or cold temperatures
• mice exhibit normal T4 levels
• in the muscle of mice fed a high-fat diet
• in response to cold exposure on a high fat diet, mice exhibit reduced body temperature and a 3-fold increase in energy expenditure compared with control mice
• under basal fed conditions
• under basal fed conditions
• at 3 months in surviving mice
• however, adiponectin levels are normal
• increased norephinephrine excretion
• 3-fold in response to cold exposure on a high fat diet

adipose tissue
• almost completely absent in severely affected mice
• at 3 months in surviving mice
• however, no macrophage infiltration is observed
• embryonic cells exhibit reduced adipogenesis compared with control cells
• at 3 months in surviving mice
• however, weights of brown adipose tissue, liver, kidney and heart are normal
• in epididymal WAT
• almost completely absent in severely affected mice
• almost completely absent in severely affected mice
• almost completely absent in severely affected mice
• almost completely absent in severely affected mice
• isoproterenol-treated white adipose tissue adipocytes exhibit reduced lipolytic response compared with control cells

growth/size/body
• at 3 months in surviving mice
• however, weights of brown adipose tissue, liver, kidney and heart are normal
• at 3 months in surviving mice
• in severely affected mice
• at 3 months in surviving mice
• however, weights of brown adipose tissue, liver, kidney and heart are normal
• at 3 months in surviving mice

behavior/neurological
• in cold-exposed mice

liver/biliary system

renal/urinary system
• increased norephinephrine excretion

integument
• almost completely absent in severely affected mice

cellular
• in the muscle of mice fed a high-fat diet





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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
07/05/2024
MGI 6.24
The Jackson Laboratory