Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse   Donating Investigator Dr. James Ntambi,   University of Wisconsin-Madison

Description
Homozygous mice are viable and fertile. Transcripts from the targeted gene are absent in homozygous liver, eyelid, skin, and white adipose tissues. In addition, the endogenous protein and enzyme activity are absent from homozygous liver tissue. Homozygous mice exhibit cutaneous abnormalities and narrow eye fissure with atrophic sebaceous and meibomian glands. Mutant mice also have reduced body adiposity, increased insulin sensitivity, increased basal and insulin-mediated glucose uptake, and are resistant to diet-induced weight gain. Homozygotes have altered hepatic glycerophospholipid profiles. Homozygous mice are not recommended for breeding as skin lesion severity may prohibit colony success. These mutant mice may be useful in studies of monounsaturated fatty acid synthesis, cholesterol homeostasis, skin disease, obesity, and diabetes.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for this strain. It should be noted that the phenotype could vary from that originally described. We will modify the strain description as published results become available.

Development
A targeting vector was designed to replace all 6 exons of the endogenous gene with a neomycin-resistant cassette. This construct was electroporated into 129/Sv-derived embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. Chimeric males were then crossed with 129/SvEv Taconic females to generate the colony. Mutant mice were backcrossed to C57BL/6J for ten generations and then made homozygous prior to arrival at The Jackson Laboratory.

Control Information

	Control
	Wild-type from the colony
	000664 C57BL/6J
Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Scd1

005956	B6;D1Lac-Scd1ab-2J/J
002304	DBA/1LacJ-Scd1ab-2J/J

View Strains carrying other alleles of Scd1     (2 strains)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

Scd1^tm1Ntam/Scd1^tm1Ntam

        involves: C57BL/6

• growth/size phenotype
• decreased susceptibility to diet-induced obesity
  • resistant to both high fat and high carbohydrate diet-induced obesity   (MGI Ref ID J:130441)
• adipose tissue phenotype
• decreased white adipose tissue amount
  • on a high fat or high carbohydrate diet WAT weights are 80% and 75% lower, respectively, compared to diet-matched wild-type mice   (MGI Ref ID J:130441)
• homeostasis/metabolism phenotype
• abnormal glucose homeostasis   (MGI Ref ID J:130441)
• • decreased circulating glucose level
    • reduced fasting plasma glucose level on a normal chow, high fat or high carbohydrate diet compared to diet-matched wild-type mice   (MGI Ref ID J:130441)
  • improved glucose tolerance
    • enhanced tolerance is seen in mice on a normal chow, high fat or high carbohydrate diet compared to diet-matched wild-type mice   (MGI Ref ID J:130441)
  • increased insulin sensitivity
    • enhanced sensitivity is seen in mice on a normal chow, high fat or high carbohydrate diet compared to diet-matched wild-type mice   (MGI Ref ID J:130441)
• decreased circulating triglyceride level
  • on a high fat or high carbohydrate diet, but not on a normal chow diet   (MGI Ref ID J:130441)
• decreased liver triglyceride level
  • decrease in palmitate and linoleate content in the liver of mice on a normal chow, high fat or high carbohydrate diet   (MGI Ref ID J:130441)
• decreased susceptibility to diet-induced obesity
  • resistant to both high fat and high carbohydrate diet-induced obesity   (MGI Ref ID J:130441)
• liver/biliary system phenotype
• decreased liver triglyceride level
  • decrease in palmitate and linoleate content in the liver of mice on a normal chow, high fat or high carbohydrate diet   (MGI Ref ID J:130441)
• decreased susceptibility to hepatic steatosis
  • protected from both high fat and high carbohydrate diet-induced fatty liver development   (MGI Ref ID J:130441)
• behavior/neurological phenotype
• increased eating behavior
  • increased in mice on a normal chow, high fat or high carbohydrate diet compared to diet-matched wild-type mice   (MGI Ref ID J:130441)

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Scd1^tm1Ntam/Scd1^tm1Ntam

        involves: 129S6/SvEvTac

• adipose tissue phenotype
• decreased white adipose tissue amount
  • especially reproductive and subcutaneous fat pads, both on high fat and normal chow diet   (MGI Ref ID J:78607)
• behavior/neurological phenotype
• polyphagia
  • consumed 25% more food than wild-type littermate controls   (MGI Ref ID J:78607)
• homeostasis/metabolism phenotype
• abnormal cholesterol homeostasis   (MGI Ref ID J:71350)
• decreased circulating insulin level
  • in fasting state, compared to wild-type littermate controls   (MGI Ref ID J:78607)
• decreased unsaturated fatty acid level
  • noted in liver, white adipose tissue, skin, eyelid   (MGI Ref ID J:71350)
• improved glucose tolerance
  • vs. wild-type littermate controls   (MGI Ref ID J:78607)
• increased circulating ketone body level   (MGI Ref ID J:78607)
• increased oxygen consumption   (MGI Ref ID J:78607)
• increased saturated fatty acid level
  • noted in liver, white adipose tissue, skin, eyelid   (MGI Ref ID J:71350)
• vision/eye phenotype
• meibomian gland atrophy   (MGI Ref ID J:71350)
• narrow eye opening
  • evident at 3 - 4weeks, and progressively more severe with age   (MGI Ref ID J:71350)
• integument phenotype
• meibomian gland atrophy   (MGI Ref ID J:71350)
• progressive hair loss
  • evident at 3-4 weeks, progressively severe with age   (MGI Ref ID J:71350)
• sebaceous gland atrophy   (MGI Ref ID J:71350)
• endocrine/exocrine gland phenotype
• meibomian gland atrophy   (MGI Ref ID J:71350)
• sebaceous gland atrophy   (MGI Ref ID J:71350)

View Research Applications

Research Applications

This mouse can be used to support research in many areas including:

Cardiovascular Research
Other
      altered fat metabolism
      altered lipoprotein profile

Dermatology Research
Other

Diabetes and Obesity Research
Insulin Receptors and Growth Factors

Endocrine Deficiency Research
Skin Defects

Internal/Organ Research
Liver Defects

Metabolism Research
Enzyme Deficiency
Lipid Metabolism

Research Tools
Dermatology Research
Diabetes and Obesity Research

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Scd1tm1Ntam
Allele Name		targeted mutation 1, James M Ntambi
Allele Type		Targeted (knock-out)
Common Name(s)		SCD1-;
Mutation Made By		Dr. Makoto Miyazaki,   University of Wisconsin-Madison
Gene Symbol and Name		Scd1, stearoyl-Coenzyme A desaturase 1
Chromosome		19
Gene Common Name(s)		AA589638; AI265570; FADS5; MSTP008; SCD; SCDOS; Scd-1; ab; asebia; expressed sequence AA589638; expressed sequence AI265570; stearoyl-CoA desaturase;
Molecular Note		The entire coding region of the gene (exons 1-6) was replaced with a neomycin resistance cassette via homologous recombination. Absence of gene expression in homozygous mutant animals was confirmed by Northern blot analysis of various tissue samples and by Western blot analysis of liver protein extracts. Enzyme activity was also undetectable in liver extracts from homozygous animals. [MGI Ref ID J:71350]

Genotyping

Genotyping Information

Genotyping Protocols

Scd1^tm1Ntam, Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Scd1^tm1Ntam related

Angrish MM; Mets BD; Jones AD; Zacharewski TR. 2012. Dietary Fat Is a Lipid Source in 2,3,7,8-Tetrachlorodibenzo-rho-Dioxin (TCDD)-Elicited Hepatic Steatosis in C57BL/6 Mice. Toxicol Sci 128(2):377-86. [PubMed: 22539624]  [MGI Ref ID J:186681]

Attie AD; Krauss RM; Gray-Keller MP; Brownlie A; Miyazaki M; Kastelein JJ; Lusis AJ; Stalenhoef AF; Stoehr JP; Hayden MR; Ntambi JM. 2002. Relationship between stearoyl-CoA desaturase activity and plasma triglycerides in human and mouse hypertriglyceridemia. J Lipid Res 43(11):1899-907. [PubMed: 12401889]  [MGI Ref ID J:123998]

Chen C; Shah YM; Morimura K; Krausz KW; Miyazaki M; Richardson TA; Morgan ET; Ntambi JM; Idle JR; Gonzalez FJ. 2008. Metabolomics reveals that hepatic stearoyl-CoA desaturase 1 downregulation exacerbates inflammation and acute colitis. Cell Metab 7(2):135-47. [PubMed: 18249173]  [MGI Ref ID J:132136]

Chu K; Miyazaki M; Man WC; Ntambi JM. 2006. Stearoyl-coenzyme A desaturase 1 deficiency protects against hypertriglyceridemia and increases plasma high-density lipoprotein cholesterol induced by liver X receptor activation. Mol Cell Biol 26(18):6786-98. [PubMed: 16943421]  [MGI Ref ID J:112300]

Dobrzyn A; Dobrzyn P; Lee SH; Miyazaki M; Cohen P; Asilmaz E; Hardie DG; Friedman JM; Ntambi JM. 2005. Stearoyl-CoA desaturase-1 deficiency reduces ceramide synthesis by downregulating serine palmitoyltransferase and increasing beta-oxidation in skeletal muscle. Am J Physiol Endocrinol Metab 288(3):E599-607. [PubMed: 15562249]  [MGI Ref ID J:96073]

Dobrzyn P; Dobrzyn A; Miyazaki M; Cohen P; Asilmaz E; Hardie DG; Friedman JM; Ntambi JM. 2004. Stearoyl-CoA desaturase 1 deficiency increases fatty acid oxidation by activating AMP-activated protein kinase in liver. Proc Natl Acad Sci U S A 101(17):6409-14. [PubMed: 15096593]  [MGI Ref ID J:89545]

Dobrzyn P; Dobrzyn A; Miyazaki M; Ntambi JM. 2010. Loss of stearoyl-CoA desaturase 1 rescues cardiac function in obese leptin-deficient mice. J Lipid Res 51(8):2202-10. [PubMed: 20363835]  [MGI Ref ID J:162951]

Dobrzyn P; Sampath H; Dobrzyn A; Miyazaki M; Ntambi JM. 2008. Loss of stearoyl-CoA desaturase 1 inhibits fatty acid oxidation and increases glucose utilization in the heart. Am J Physiol Endocrinol Metab 294(2):E357-64. [PubMed: 18042664]  [MGI Ref ID J:133284]

Flowers JB; Rabaglia ME; Schueler KL; Flowers MT; Lan H; Keller MP; Ntambi JM; Attie AD. 2007. Loss of stearoyl-CoA desaturase-1 improves insulin sensitivity in lean mice but worsens diabetes in leptin-deficient obese mice. Diabetes 56(5):1228-39. [PubMed: 17369521]  [MGI Ref ID J:122081]

Flowers MT; Groen AK; Oler AT; Keller MP; Choi Y; Schueler KL; Richards OC; Lan H; Miyazaki M; Kuipers F; Kendziorski CM; Ntambi JM; Attie AD. 2006. Cholestasis and hypercholesterolemia in SCD1-deficient mice fed a low-fat, high-carbohydrate diet. J Lipid Res 47(12):2668-80. [PubMed: 17005996]  [MGI Ref ID J:117233]

Flowers MT; Keller MP; Choi Y; Lan H; Kendziorski C; Ntambi JM; Attie AD. 2008. Liver gene expression analysis reveals endoplasmic reticulum stress and metabolic dysfunction in SCD1-deficient mice fed a very low-fat diet. Physiol Genomics 33(3):361-72. [PubMed: 18381840]  [MGI Ref ID J:145309]

Hirschey MD; Shimazu T; Jing E; Grueter CA; Collins AM; Aouizerat B; Stancakova A; Goetzman E; Lam MM; Schwer B; Stevens RD; Muehlbauer MJ; Kakar S; Bass NM; Kuusisto J; Laakso M; Alt FW; Newgard CB; Farese RV Jr; Kahn CR; Verdin E. 2011. SIRT3 deficiency and mitochondrial protein hyperacetylation accelerate the development of the metabolic syndrome. Mol Cell 44(2):177-90. [PubMed: 21856199]  [MGI Ref ID J:178653]

Lee SH; Dobrzyn A; Dobrzyn P; Rahman SM; Miyazaki M; Ntambi JM. 2004. Lack of stearoyl-CoA desaturase 1 upregulates basal thermogenesis but causes hypothermia in a cold environment. J Lipid Res 45(9):1674-82. [PubMed: 15210843]  [MGI Ref ID J:93618]

Miyazaki M; Dobrzyn A; Man WC; Chu K; Sampath H; Kim HJ; Ntambi JM. 2004. Stearoyl-CoA desaturase 1 gene expression is necessary for fructose-mediated induction of lipogenic gene expression by sterol regulatory element-binding protein-1c-dependent and -independent mechanisms. J Biol Chem 279(24):25164-71. [PubMed: 15066988]  [MGI Ref ID J:90732]

Miyazaki M; Dobrzyn A; Sampath H; Lee SH; Man WC; Chu K; Peters JM; Gonzalez FJ; Ntambi JM. 2004. Reduced adiposity and liver steatosis by stearoyl-CoA desaturase deficiency are independent of peroxisome proliferator-activated receptor-alpha. J Biol Chem 279(33):35017-24. [PubMed: 15180999]  [MGI Ref ID J:92232]

Miyazaki M; Flowers MT; Sampath H; Chu K; Otzelberger C; Liu X; Ntambi JM. 2007. Hepatic stearoyl-CoA desaturase-1 deficiency protects mice from carbohydrate-induced adiposity and hepatic steatosis. Cell Metab 6(6):484-96. [PubMed: 18054317]  [MGI Ref ID J:130441]

Miyazaki M; Gomez FE; Ntambi JM. 2002. Lack of stearoyl-CoA desaturase-1 function induces a palmitoyl-CoA Delta6 desaturase and represses the stearoyl-CoA desaturase-3 gene in the preputial glands of the mouse. J Lipid Res 43(12):2146-54. [PubMed: 12454277]  [MGI Ref ID J:80688]

Miyazaki M; Kim HJ; Man WC; Ntambi JM. 2001. Oleoyl-CoA is the major de novo product of stearoyl-CoA desaturase 1 gene isoform and substrate for the biosynthesis of the Harderian gland 1-alkyl-2,3-diacylglycerol. J Biol Chem 276(42):39455-61. [PubMed: 11500518]  [MGI Ref ID J:132900]

Miyazaki M; Kim YC; Ntambi JM. 2001. A lipogenic diet in mice with a disruption of the stearoyl-CoA desaturase 1 gene reveals a stringent requirement of endogenous monounsaturated fatty acids for triglyceride synthesis. J Lipid Res 42(7):1018-24. [PubMed: 11441127]  [MGI Ref ID J:70344]

Miyazaki M; Man WC; Ntambi JM. 2001. Targeted disruption of stearoyl-CoA desaturase1 gene in mice causes atrophy of sebaceous and meibomian glands and depletion of wax esters in the eyelid. J Nutr 131(9):2260-8. [PubMed: 11533264]  [MGI Ref ID J:71350]

Miyazaki M; Sampath H; Liu X; Flowers MT; Chu K; Dobrzyn A; Ntambi JM. 2009. Stearoyl-CoA desaturase-1 deficiency attenuates obesity and insulin resistance in leptin-resistant obese mice. Biochem Biophys Res Commun 380(4):818-22. [PubMed: 19338759]  [MGI Ref ID J:147343]

Ntambi JM; Miyazaki M; Stoehr JP; Lan H; Kendziorski CM; Yandell BS; Song Y; Cohen P; Friedman JM; Attie AD. 2002. Loss of stearoyl-CoA desaturase-1 function protects mice against adiposity. Proc Natl Acad Sci U S A 99(17):11482-6. [PubMed: 12177411]  [MGI Ref ID J:78607]

Rahman SM; Dobrzyn A; Dobrzyn P; Lee SH; Miyazaki M; Ntambi JM. 2003. Stearoyl-CoA desaturase 1 deficiency elevates insulin-signaling components and down-regulates protein-tyrosine phosphatase 1B in muscle. Proc Natl Acad Sci U S A 100(19):11110-5. [PubMed: 12960377]  [MGI Ref ID J:99738]

Sampath H; Miyazaki M; Dobrzyn A; Ntambi JM. 2007. Stearoyl-CoA desaturase-1 mediates the pro-lipogenic effects of dietary saturated fat. J Biol Chem 282(4):2483-93. [PubMed: 17127673]  [MGI Ref ID J:120295]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & Husbandry	When maintaining a live colony, heterozygous mice are bred. Homozygous mice are not recommended for breeding as skin lesion severity may prohibit colony success.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls

Control Information

	Control
	Wild-type from the colony
	000664 C57BL/6J
Considerations for Choosing Controls
Control Pricing Information for Genetically Engineered Mutant Strains.

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

See Terms of Use tab for General Terms and Conditions

The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX^® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX^® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX^® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.

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Terms of Use

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JAX^® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

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