All Phenotypes Lepr<tm1Jke> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Lepr^tm1Jke/Lepr^tm1Jke	involves: 129X1/SvJ	MGI:5620891
hm2	Lepr^tm1Jke/Lepr^tm1Jke	involves: 129X1/SvJ * C57BL/6J	MGI:5426232
cn3	Lepr^tm1Jke/Lepr^tm1Jke Tg(Pomc1-cre)16Lowl/0	involves: 129X1/SvJ * C57BL/6J * FVB/N	MGI:5426233
cx4	Gcgr^tm1Mjch/Gcgr^tm1Mjch Lepr^tm1Jke/Lepr^tm1Jke	involves: 129 * 129X1/SvJ * C57BL/6J * SJL	MGI:5620894

Allelic Composition	Lepr^tm1Jke/Lepr^tm1Jke
Genetic Background	involves: 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lepr^tm1Jke mutation (2 available); any Lepr mutation (122 available)

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

growth/size/body

obese ( J:216393 )

• mice become obese at 21-28 days of age

homeostasis/metabolism

hyperglycemia ( J:216393 )

• mice become hyperglycemic between 5 and 10 weeks of age

increased circulating insulin level ( J:216393 )

• mice become hyperinsulinemic at 10-14 days of age

increased liver triglyceride level ( J:216393 )

increased susceptibility to non-insulin-dependent diabetes ( J:216393 )

• mice are diabetic, with high mean glucose concentration despite extreme hyperinsulinemia

liver/biliary system

increased liver triglyceride level ( J:216393 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
type 2 diabetes mellitus		DOID:9352	OMIM:125853 OMIM:601283 OMIM:601407 OMIM:603694 OMIM:608036	J:216393

Allelic Composition	Lepr^tm1Jke/Lepr^tm1Jke
Genetic Background	involves: 129X1/SvJ * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lepr^tm1Jke mutation (2 available); any Lepr mutation (122 available)

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

homeostasis/metabolism

increased circulating leptin level ( J:184572 )

increased circulating cholesterol level ( J:184572 )

increased circulating triglyceride level ( J:184572 )

decreased carbon dioxide production ( J:184572 )

decreased oxygen consumption ( J:184572 )

decreased respiratory quotient ( J:184572 )

abnormal glucose homeostasis ( J:184572 )

• insulin-stimulated glucose disposal is impaired compared to in wild-type mice

increased insulin secretion ( J:184572 )

• in the pancreas

hyperglycemia ( J:184572 )

increased circulating glucagon level ( J:184572 )

• in male mice at 12 and 20 weeks in the fed, fasted and carbohydrate-refed condition

increased circulating insulin level ( J:184572 )

abnormal gluconeogenesis ( J:184572 )

• basal and insulin-stimulated

increased insulin sensitivity ( J:184572 )

increased liver triglyceride level ( J:184572 )

behavior/neurological

abnormal eating behavior ( J:184572 )

decreased locomotor activity ( J:184572 )

• during the dark phase

growth/size/body

obese ( J:184572 )

endocrine/exocrine glands

increased insulin secretion ( J:184572 )

• in the pancreas

liver/biliary system

increased liver triglyceride level ( J:184572 )

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

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:184572 )

N	• mice exhibit normal circulating glucagon levels in the fed and carbohydrate-refed state

increased circulating leptin level ( J:184572 )

• compared with wild-type mice

decreased circulating cholesterol level ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

increased circulating cholesterol level ( J:184572 )

• compared with wild-type mice

decreased circulating triglyceride level ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

increased circulating triglyceride level ( J:184572 )

• compared with wild-type mice

decreased carbon dioxide production ( J:184572 )

• compared with wild-type mice

increased carbon dioxide production ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

decreased oxygen consumption ( J:184572 )

• compared with wild-type mice

increased oxygen consumption ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

increased respiratory quotient ( J:184572 )

• compared with wild-type mice

abnormal glucose homeostasis ( J:184572 )

• mice exhibit normal basal glucose turnover compared with Lepr^tm1Jke homozygotes

• insulin-stimulated glucose disposal is impaired compared to in wild-type mice

• however, mice exhibit normal circulating glucose levels at 6, 8 and 12 weeks

increased insulin secretion ( J:184572 )

• in the pancreas compared with wild-type mice

decreased circulating glucose level ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

decreased circulating insulin level ( J:184572 )

• at 8 and 12 weeks compared with Lepr^tm1Jke homozygotes

increased circulating insulin level ( J:184572 )

• compared with wild-type mice

increased insulin sensitivity ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

decreased liver triglyceride level ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

increased liver triglyceride level ( J:184572 )

• compared with wild-type mice

growth/size/body

decreased body weight ( J:184572 )

• in male mice after 12 weeks compared with Lepr^tm1Jke homozygotes

obese ( J:184572 )

• in male mice between 4 and 12 weeks less severe after 12 weeks compared with wild-type mice

• in female mice

behavior/neurological

abnormal eating behavior ( J:184572 )

• compared with wild-type mice

hyperactivity ( J:184572 )

• during the dark phase compared with wild-type mice

adipose tissue

decreased total body fat amount ( J:184572 )

• in male mice at 20 weeks compared with Lepr^tm1Jke homozygotes

increased total body fat amount ( J:184572 )

• in male mice at 12 and 20 weeks compared with wild-type mice

endocrine/exocrine glands

increased insulin secretion ( J:184572 )

• in the pancreas compared with wild-type mice

liver/biliary system

decreased liver triglyceride level ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

increased liver triglyceride level ( J:184572 )

• compared with wild-type mice

Allelic Composition	Gcgr^tm1Mjch/Gcgr^tm1Mjch Lepr^tm1Jke/Lepr^tm1Jke
Genetic Background	involves: 129 * 129X1/SvJ * C57BL/6J * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gcgr^tm1Mjch mutation (0 available); any Gcgr mutation (8 available)
Lepr^tm1Jke mutation (2 available); any Lepr mutation (122 available)

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

growth/size/body

obese ( J:216393 )

• mice are obese but weight less than single Lepr homozygotes

• however, glucose and insulin levels are in the normal range

homeostasis/metabolism

increased liver triglyceride level ( J:216393 )

• increase in liver triacylglycerol levels but to a lower extent than in single Lepr homozygotes

liver/biliary system

increased liver triglyceride level ( J:216393 )

• increase in liver triacylglycerol levels but to a lower extent than in single Lepr homozygotes

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