All Phenotypes Ptpn1<tm2Bbk> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Ptpn1^tm2Bbk/Ptpn1^tm2Bbk Ptpn2^tm1.1Ttig/Ptpn2^tm1.1Ttig Tg(Nes-cre)1Kln/0	involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL	MGI:5304839
cn2	Ptpn1^tm2Bbk/Ptpn1^tm2Bbk Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺	involves: 129S4/SvJae * C57BL/6 * DBA/2	MGI:3664093
cn3	Ptpn1^tm2Bbk/Ptpn1^tm2Bbk Tg(Nes-cre)1Kln/0	involves: 129S4/SvJae * C57BL/6 * SJL	MGI:3664097
cn4	Ptpn1^tm2Bbk/Ptpn1⁺ Tg(Nes-cre)1Kln/0	involves: 129S4/SvJae * C57BL/6 * SJL	MGI:3664098

Allelic Composition	Ptpn1^tm2Bbk/Ptpn1^tm2Bbk Ptpn2^tm1.1Ttig/Ptpn2^tm1.1Ttig Tg(Nes-cre)1Kln/0
Genetic Background	involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptpn1^tm2Bbk mutation (1 available); any Ptpn1 mutation (36 available)
Ptpn2^tm1.1Ttig mutation (0 available); any Ptpn2 mutation (43 available)
Tg(Nes-cre)1Kln mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

abnormal homeostasis ( J:179621 )

• whether fed standard chow or a high-fat diet, leptin-treated mice exhibit enhanced leptin sensitivity compared with wild-type mice

decreased circulating leptin level ( J:179621 )

• when fed standard chow

increased energy expenditure ( J:179621 )

• when fed standard chow

decreased susceptibility to diet-induced obesity ( J:179621 )

• when fed a high-fat diet

increased oxygen consumption ( J:179621 )

• when fed standard chow

abnormal respiratory quotient ( J:179621 )

• when fed standard chow, respiratory exchange ratio is decreased in the light cycle and increased in the dark cycle compared with wild-type mice

abnormal glucose homeostasis ( J:179621 )

• glucose homeostasis is improved in mice fed a high-fat diet compared to in wild-type mice

decreased circulating glucose level ( J:179621 )

• in fasted mice fed standard chow

increased insulin sensitivity ( J:179621 )

• when fed standard chow

growth/size/body

decreased body weight ( J:179621 )

• when fed standard chow

decreased body length ( J:179621 )

• when fed standard chow

decreased susceptibility to diet-induced obesity ( J:179621 )

• when fed a high-fat diet

behavior/neurological

abnormal eating behavior ( J:179621 )

• when fed standard chow

Allelic Composition	Ptpn1^tm2Bbk/Ptpn1^tm2Bbk Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
Genetic Background	involves: 129S4/SvJae * C57BL/6 * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptpn1^tm2Bbk mutation (1 available); any Ptpn1 mutation (36 available)
Speer6-ps1^{Tg(Alb-cre)21Mgn} mutation (6 available); any Speer6-ps1 mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

growth/size/body region phenotype ( J:111969 )

N	• mice with liver-specific Ptpn1 deletion show similar body weight to Ptpn1-sufficient controls

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

decreased body weight ( J:111969 )

• male neuronal Ptpn1-deficient mice show significantly reduced body weight on a high fat diet compared to control Ptpn1-sufficient (undeleted Ptpn1^tm2Bbk homozygous) animals between 9 and 17 weeks of age; females show reduced body weight but less markedly so than control female mice on a high fat diet

• neuronal Ptpn1-deficient mice also weigh less than controls when fed a regular chow diet (decrease of 4.5% fat by weight)

decreased susceptibility to diet-induced obesity ( J:179621 )

• when fed a high-fat diet

homeostasis/metabolism

abnormal homeostasis ( J:179621 )

• whether fed standard chow or a high-fat diet, leptin-treated mice exhibit enhanced leptin sensitivity compared with wild-type mice

decreased susceptibility to diet-induced obesity ( J:179621 )

• when fed a high-fat diet

decreased circulating glucose level ( J:111969 )

• mutants have lower fed blood glucose on regular chow and HFD vs controls

increased oxygen consumption ( J:111969 )

decreased respiratory quotient ( J:111969 )

• mice display greater oxygen consumption and a decreased respiratory quotient

improved glucose tolerance ( J:111969 )

• male mice at 8-10 weeks of age show enhanced glucose tolerance compared to littermate comtrols

increased insulin sensitivity ( J:111969 , J:179621 )

• male mice at 8-10 weeks of age show improved insulin sensitivity compared to littermate controls (J:111969)

• female mice also show significantly improved insulin sensitivity even though weight at 8 weeks of age is the same as controls; insulin sensitivity and glucose tolerance are similar to whole body deficient Ptpn1^tm1Bbk mice (J:111969)

abnormal hormone level ( J:111969 )

• leptin protein is elevated in white adipose tissue of these mice, suggesting that increased serum leptin levels are due to increased adipocyte leptin production

decreased circulating insulin level ( J:111969 )

• mutants have lower seurm insulin levels on regular chow and HFD vs controls

decreased circulating leptin level ( J:179621 )

increased circulating leptin level ( J:111969 )

• neuronal Ptpn1-deficient mice show increased serum leptin levels (2.3 -fold on a regular chow diet, 4.4-fold higher on a HFD) compared to Ptpn1-undeleted littermates, detected 4 weeks after birth

increased circulating adiponectin level ( J:111969 )

• adiponectin levels are elevated and resistin levels are unexpectedly normal in mutants on regular and HFD diets

decreased triglyceride level ( J:111969 )

• mice show reduced adiposity after high-fat feeding based on lower carcass triglyceride content compared to controls

behavior/neurological

abnormal food intake ( J:111969 )

• intake is slightly less in mutants than controls

• when treated with leptin twice per day over a 60 hour period, male mice show enhanced suppression of food intake vs controls

decreased food intake ( J:111969 )

• male mice injected with leptin show decreased food intake during the period of treatment compared to controls

abnormal motor capabilities/coordination/movement ( J:111969 )

• neuronal Ptpn1-deficient mice display increased ambulatory movement vs control

skeleton

decreased bone mineral density ( J:111969 )

• when treated with leptin twice per day over a 60 hour period, male mice show reduced bone mineral density

adipose tissue

abnormal fat pad morphology ( J:111969 )

Allelic Composition	Ptpn1^tm2Bbk/Ptpn1⁺ Tg(Nes-cre)1Kln/0
Genetic Background	involves: 129S4/SvJae * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptpn1^tm2Bbk mutation (1 available); any Ptpn1 mutation (36 available)
Tg(Nes-cre)1Kln mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

decreased body weight ( J:111969 )

• male mice heterozygous for Ptpn1^tm2Bbk show reduced body weight on a high fat diet between 9 and 17 weeks of age compared to Ptpn1-sufficient controls

homeostasis/metabolism

decreased circulating glucose level ( J:111969 )

• mutants have lower fed blood glucose on regular chow and HFD vs controls

decreased circulating insulin level ( J:111969 )

• mutants have lower seurm insulin levels on regular chow and HFD vs controls

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