All Phenotypes Dgat1<tm1Far> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Dgat1^tm1Far/Dgat1^tm1Far	B6J.129S4-Dgat1^tm1Far	MGI:5644488
hm2	Dgat1^tm1Far/Dgat1^tm1Far	involves: 129S4/SvJae * C57BL/6J	MGI:3622547
cx3	Adipoq^tm1Far/Adipoq^tm1Far Dgat1^tm1Far/Dgat1^tm1Far	involves: 129S4/SvJae * C57BL/6J	MGI:3664726

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

endocrine/exocrine glands

decreased mammary gland epithelial cell proliferation ( J:128259 )

• on day 15 of pregnancy (P15), BrdU labeling shows a 40% reduction in proliferating nuclei in mutant mammary epithelium

• in contrast, levels of apoptosis remain similar to those of wild-type controls at P18, as shown by TUNEL staining

abnormal mammary gland development ( J:128259 )

• whole wild-type mammary glands transplanted into mutant recipient mice show fully developed lobuloalveolar structures and visible milk droplets whereas whole mutant mammary glands transplanted into wild-type recipient mice fail to develop normally

abnormal branching of the mammary ductal tree ( J:128259 )

• at P15, mutant mammary glands show a slight decrease in ductal structures

• however, ductal side branching appears normal at P8

abnormal mammary gland growth during lactation ( J:128259 )

• on day 1 of lactation ( L1), mutant glands show a ~25% reduction in epithelial structures and a ~60% reduction in luminal expansion

impaired mammary gland growth during pregnancy ( J:128259 )

• at P15, mutant mammary glands show a slight decrease in ductal structures, suggesting a developmental delay

• by P18, alveolar development is reduced and mutant glands show a ~25% reduction in epithelial structures and a ~60% reduction in luminal expansion

abnormal mammary gland epithelium morphology ( J:128259 )

• female homozygotes show impaired differentiation of mammary gland epithelium in late pregnancy

• transplantation of mutant epithelium to wild-type mammary fat pads results in apparently normal epithelial growth, whereas transplantation of wild-type epithelium to mutant fat pads leads to underdeveloped and poorly differentiated epithelium

abnormal mammary gland alveolus morphology ( J:128259 )

• by P18, mutant lobuloalveolar structures are less developed relative to wild-type controls

• however, formation of the initial alveolar buds appears normal at P8

abnormal milk composition ( J:128259 )

• in mutant mammary glands, expression of whey acidic protein (WAP), a late differentiation marker, is absent at P18 and reduced at L1

• in contrast, expression of beta-casein, an early differentiation marker, is similar to that in wild-type glands

lactation failure ( J:128259 )

• milk production is totally absent, even after stimulation by oxytocin or by a second pregnancy

• pups born to female homozygotes die shortly after birth with no milk stripes in their stomachs

• however, pups fostered to lactating wild-type females suckle and develop normally

integument

decreased mammary gland epithelial cell proliferation ( J:128259 )

• on day 15 of pregnancy (P15), BrdU labeling shows a 40% reduction in proliferating nuclei in mutant mammary epithelium

• in contrast, levels of apoptosis remain similar to those of wild-type controls at P18, as shown by TUNEL staining

abnormal mammary gland development ( J:128259 )

abnormal branching of the mammary ductal tree ( J:128259 )

• at P15, mutant mammary glands show a slight decrease in ductal structures

• however, ductal side branching appears normal at P8

abnormal mammary gland growth during lactation ( J:128259 )

• on day 1 of lactation ( L1), mutant glands show a ~25% reduction in epithelial structures and a ~60% reduction in luminal expansion

impaired mammary gland growth during pregnancy ( J:128259 )

• at P15, mutant mammary glands show a slight decrease in ductal structures, suggesting a developmental delay

• by P18, alveolar development is reduced and mutant glands show a ~25% reduction in epithelial structures and a ~60% reduction in luminal expansion

abnormal mammary gland epithelium morphology ( J:128259 )

• female homozygotes show impaired differentiation of mammary gland epithelium in late pregnancy

abnormal mammary gland alveolus morphology ( J:128259 )

• by P18, mutant lobuloalveolar structures are less developed relative to wild-type controls

• however, formation of the initial alveolar buds appears normal at P8

abnormal milk composition ( J:128259 )

• in mutant mammary glands, expression of whey acidic protein (WAP), a late differentiation marker, is absent at P18 and reduced at L1

• in contrast, expression of beta-casein, an early differentiation marker, is similar to that in wild-type glands

lactation failure ( J:128259 )

• milk production is totally absent, even after stimulation by oxytocin or by a second pregnancy

• pups born to female homozygotes die shortly after birth with no milk stripes in their stomachs

• however, pups fostered to lactating wild-type females suckle and develop normally

reproductive system

impaired mammary gland growth during pregnancy ( J:128259 )

• at P15, mutant mammary glands show a slight decrease in ductal structures, suggesting a developmental delay

• by P18, alveolar development is reduced and mutant glands show a ~25% reduction in epithelial structures and a ~60% reduction in luminal expansion

adipose tissue

decreased mammary fat pad weight ( J:128259 )

• the weights of mutant mammary fat pads are similar to those of wild-type mice during pregnancy, but are decreased at L1, probably due to lack of milk production

cellular

decreased mammary gland epithelial cell proliferation ( J:128259 )

• on day 15 of pregnancy (P15), BrdU labeling shows a 40% reduction in proliferating nuclei in mutant mammary epithelium

• in contrast, levels of apoptosis remain similar to those of wild-type controls at P18, as shown by TUNEL staining

Allelic Composition	Dgat1^tm1Far/Dgat1^tm1Far
Genetic Background	involves: 129S4/SvJae * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dgat1^tm1Far mutation (1 available); any Dgat1 mutation (32 available)

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

Enhanced epidermal response to topical retinol treatment in Dgat1^tm1Far/Dgat1^tm1Far mice

homeostasis/metabolism

decreased susceptibility to diet-induced obesity ( J:61885 )

• when fed a high-fat diet, mutant mice were resistant to obesity

• mice fed a chow diet had similar body weights, but the weight of the total fat pads in mutant mice was lower than control

• mutant mice has higher metabolic rates both on a chow diet and on a high-fat diet

decreased circulating glucose level ( J:111346 )

• after high-fat diet for 8 weeks, mice have decreased blood glucose after an overnight fast vs controls

decreased circulating leptin level ( J:111346 )

• serum leptin levels are significantly lower than in Dgat1-sufficient animals regardless of Adipoq genotype (4.2 ng/ml vs ~17.7 ng/ml in Dgat1-suffcient)

increased oxygen consumption ( J:111346 )

• mice fed a higher fat diet have higher levels of oxygen consumption than Dgat1-sufficient mice

improved glucose tolerance ( J:111346 )

• after glucose challenge, improved glucose tolerance compared to wild-type controls is seen; Dgat1-deficiency improves glucose tolerance by ~30-35% vs controls

increased insulin sensitivity ( J:61885 )

• tended to have lower glucose and insulin levels after a glucose tolerance test

decreased liver cholesterol level ( J:111346 )

• after receiving a high-fat diet for 20 weeks, hepatic cholesterol ester levels are markedly reduced vs controls

decreased liver triglyceride level ( J:111346 )

• after receiving a high-fat diet for 20 weeks, hepatic triglyceride levels are markedly reduced vs controls

abnormal vitamin A level ( J:147611 )

• levels of unesterified retinol in skin are elevated 22% on a normal diet

• all trans retinoic acids in skin are increased 40%

• serum retinol and liver retinoid levels are normal

behavior/neurological

hyperactivity ( J:61885 )

• on the high-fat diet, mutant mice were twice as active as wild-type mice

endocrine/exocrine glands

lactation failure ( J:61885 )

• females had a complete absence of milk production

adipose tissue

decreased percent body fat/body weight ( J:111346 )

• lower than Dgat1-sufficient mice

growth/size/body

decreased body weight ( J:111346 )

• when Dgat1-deficient, Adipoq-sufficient mice are weaned onto a high-fat diet, they show decreased body weight over 20 weeks vs wild-type controls

decreased susceptibility to diet-induced obesity ( J:61885 )

• when fed a high-fat diet, mutant mice were resistant to obesity

• mice fed a chow diet had similar body weights, but the weight of the total fat pads in mutant mice was lower than control

• mutant mice has higher metabolic rates both on a chow diet and on a high-fat diet

liver/biliary system

decreased liver cholesterol level ( J:111346 )

• after receiving a high-fat diet for 20 weeks, hepatic cholesterol ester levels are markedly reduced vs controls

decreased liver triglyceride level ( J:111346 )

• after receiving a high-fat diet for 20 weeks, hepatic triglyceride levels are markedly reduced vs controls

decreased susceptibility to diet-induced hepatic steatosis ( J:111346 )

• when fed a high fat diet for 20 weeks, mice show significantly less hepatic steatosis vs wild-type controls

integument

lactation failure ( J:61885 )

• females had a complete absence of milk production

abnormal coat/ hair morphology ( J:147611 )

alopecia ( J:147611 )

• manifests as a prominent bald spot in the dorsal caudal region at 9 weeks

• hair regrows but patchy alopecia always redevelops in variable locations and persists in 5 to 7 month old mice

• maintainance on a retinoid deficient diet prevents alopecia

sparse hair ( J:147611 )

• generalized hair thinning at 5 to 7 months of age

abnormal hair cycle ( J:147611 )

abnormal hair cycle anagen phase ( J:147611 )

• prolonged first anagen

• early entrance into second anagen

abnormal hair shedding ( J:147611 )

• increased shedding

abnormal epidermal layer morphology ( J:147611 )

epidermal hyperplasia ( J:147611 )

• four days after a single application of retinol to shaved skin

thick epidermis ( J:147611 )

• four days after a single application of retinol to shaved skin

reddish skin ( J:147611 )

• due to three consecutive days of retinol application

scaly skin ( J:147611 )

• due to three consecutive days of retinol application

skin lesions ( J:147611 )

• cracking and crusty lesions

• due to three consecutive days of retinol application

abnormal skin condition ( J:147611 )

Allelic Composition	Adipoq^tm1Far/Adipoq^tm1Far Dgat1^tm1Far/Dgat1^tm1Far
Genetic Background	involves: 129S4/SvJae * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adipoq^tm1Far mutation (0 available); any Adipoq mutation (40 available)
Dgat1^tm1Far mutation (1 available); any Dgat1 mutation (32 available)

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

adipose tissue

decreased total body fat amount ( J:111346 )

• lower than Dgat1-sufficient mice

decreased percent body fat/body weight ( J:111346 )

• lower than Dgat1-sufficient mice

behavior/neurological

increased food intake ( J:111346 )

• mice show significant increase in food intake compared to other genotypes

endocrine/exocrine glands

abnormal lactation ( J:111346 )

• females display a lactation defect similar to Dgat1-deficient mice

growth/size/body

decreased body weight ( J:111346 )

• when Dgat1-deficient, Adipoq-deficient mice are weaned onto a high-fat diet, they show decreased body weight over 20 weeks similar to Dgat1-deficient, Adipoq-sufficient mice

homeostasis/metabolism

decreased circulating glucose level ( J:111346 )

• after high-fat diet for 8 weeks, mice are completely protected from diet-induced fasting increases in blood glucose after an overnight fast; levels are similar to Dgat1-deficient mice

decreased circulating leptin level ( J:111346 )

• serum leptin levels are significantly lower than in Dgat1-sufficient animals regardless of Adipoq genotype (2.5 ng/ml vs ~17.7 ng/ml in Dgat1-suffcient)

increased oxygen consumption ( J:111346 )

• mice fed a higher fat diet have higher levels of oxygen consumption than Dgat1-sufficient mice

abnormal glucose tolerance ( J:111346 )

• after glucose challenge, mice show improved glucose tolerance compared to Adipoq-deficient mice but slightly more impaired tolerance than Dgat1-deficient mice; Dgat1-deficiency improves glucose tolerance by ~30-35% vs controls while Adipoq deficiency impairs glucose tolerance by ~25%

decreased liver cholesterol level ( J:111346 )

• after receiving a high-fat diet for 20 weeks, hepatic cholesterol ester levels are markedly reduced vs controls

decreased liver triglyceride level ( J:111346 )

• after receiving a high-fat diet for 20 weeks, hepatic triglyceride levels are markedly reduced vs controls

liver/biliary system

decreased liver cholesterol level ( J:111346 )

• after receiving a high-fat diet for 20 weeks, hepatic cholesterol ester levels are markedly reduced vs controls

decreased liver triglyceride level ( J:111346 )

• after receiving a high-fat diet for 20 weeks, hepatic triglyceride levels are markedly reduced vs controls

decreased susceptibility to diet-induced hepatic steatosis ( J:111346 )

• when fed a high fat diet for 20 weeks, mice show significantly less hepatic steatosis vs wild-type controls

integument

abnormal lactation ( J:111346 )

• females display a lactation defect similar to Dgat1-deficient mice

abnormal coat appearance ( J:111346 )

• double mutants have dry fur similar to Dgat1-deficient mice

premature hair loss ( J:111346 )

• similar to Dgat1-deficient mice

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