Strain Name:

B6.129S4-Lpltm1Ijg/J

Stock Number:

006503

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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.
Specieslaboratory mouse
GenerationN7F3pN1
Generation Definitions
 
Donating Investigator Ira Goldberg,   Columbia University

Description
These mice possess loxP sites on either side of exon 1 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. These mice may be useful for cardiovascular studies (such as lipid metabolism and fat storage) and obesity research.

For example, when crossed to a strain expressing Cre recombinase in cardiac muscle cells (see Stock No. 011038), this mutant mouse strain may be useful in studies of cardiac lipid metabolism.

Development
A loxP site flanked targeting vector containing neomycin resistance and thymidine kinase genes was utilized in the construction of this mutant. This selection cassette was inserted upstream of exon 1 of the targeted gene, and another loxP site was inserted in the first intron. This construct was electroporated into 129S4/SvJae derived J1 embryonic stem (ES) cells which were transiently transfected with a Cre recombinase vector to remove the selection cassette. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric mice were backcrossed to C57BL/6 for 6 generations.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Additional Web Information

Introduction to Cre-lox technology

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Hyperlipidemia, Familial Combined; FCHL   (LPL)
Hyperlipoproteinemia, Type I   (LPL)
Lipoprotein Lipase; LPL   (LPL)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

The following phenotype relates to a compound genotype created using this strain.
Contact JAX® Services jaxservices@jax.org for customized breeding options.

Lpltm1Ijg/Lpltm1Ijg Tg(Myh6-cre)2182Mds/0

        involves: FVB/N   (conditional)
  • mortality/aging
  • increased sensitivity to induced morbidity/mortality
    • all mutants subjected to abdominal aortic constriction (AbAC) die within 2 days whereas controls survive   (MGI Ref ID J:110484)
  • cardiovascular system phenotype
  • abnormal cardiovascular system physiology
    • hearts from both 4-5 month old males and females exhibit higher rates of glycolysis and glucose oxidation   (MGI Ref ID J:110484)
    • palmitate oxidation rates in male and female hearts are reduced by 52 and 40%, respectively, indicating reduction in fatty acid utilization   (MGI Ref ID J:110484)
    • heart uptake of VLDL triglycerides is decreased by 49% and uptake of palmitate, a free fatty acid, is increased by 56% in females   (MGI Ref ID J:110484)
    • male, but not female, hearts show a reduction in cardiac power   (MGI Ref ID J:110484)
    • abnormal cardiac cell glucose uptake
      • myocardial basal glucose uptake is increased 5.5-fold   (MGI Ref ID J:110484)
    • decreased cardiac muscle contractility
      • 6-month old mutants exhibit an increase in left ventricular systolic dimension and a decrease in fractional shortening under basal conditions   (MGI Ref ID J:110484)
    • increased left ventricle diastolic pressure
      • mutants subjected to abdominal aortic constriction exhibit an increase in left ventricular end diastolic pressure that is not observed in banded controls   (MGI Ref ID J:110484)
    • increased left ventricle systolic pressure
      • mutants subjected to abdominal aortic constriction exhibit a greater increase in left ventricular systolic pressure than banded controls   (MGI Ref ID J:110484)
  • cardiac fibrosis
    • hearts from non-stressed 4-5 month old males, but not females, show increased fibrosis as indicated by Trichrome staining; fibrosis is both interstitial and perivascular   (MGI Ref ID J:110484)
    • cardiac interstitial fibrosis
      • seen in non-stressed 4-5 month old males   (MGI Ref ID J:110484)
  • homeostasis/metabolism phenotype
  • abnormal glucose homeostasis
    • hearts from both 4-5 month old males and females exhibit higher rates of glycolysis and glucose oxidation   (MGI Ref ID J:110484)
  • cardiac fibrosis
    • hearts from non-stressed 4-5 month old males, but not females, show increased fibrosis as indicated by Trichrome staining; fibrosis is both interstitial and perivascular   (MGI Ref ID J:110484)
    • cardiac interstitial fibrosis
      • seen in non-stressed 4-5 month old males   (MGI Ref ID J:110484)
  • increased circulating triglyceride level
    • 4 month old females show elevated plasma triglyceride levels, however plasma cholesterol, free fatty acid, and glucose levels are normal   (MGI Ref ID J:110484)
  • muscle phenotype
  • abnormal cardiac cell glucose uptake
    • myocardial basal glucose uptake is increased 5.5-fold   (MGI Ref ID J:110484)
  • decreased cardiac muscle contractility
    • 6-month old mutants exhibit an increase in left ventricular systolic dimension and a decrease in fractional shortening under basal conditions   (MGI Ref ID J:110484)
  • cellular phenotype
  • abnormal cardiac cell glucose uptake
    • myocardial basal glucose uptake is increased 5.5-fold   (MGI Ref ID J:110484)

Lpltm1Ijg/Lpltm1Ijg Tg(Myh6-cre)2182Mds/?

        involves: C57BL/6   (conditional)
  • homeostasis/metabolism phenotype
  • abnormal glucose homeostasis
    • basal glucose uptake by the heart increased 8 fold   (MGI Ref ID J:90737)
    • tendency for insulin stimulated glucose uptake by the heart to increase somewhat   (MGI Ref ID J:90737)
  • abnormal lipid level
    • heart uptake of VLDL decreased by 72%   (MGI Ref ID J:90737)
    • abnormal fatty acid level
      • heart content of fatty acids decreased   (MGI Ref ID J:90737)
      • postprandial levels tended to remain elevated   (MGI Ref ID J:90737)
    • increased triglyceride level
      • plasma triglyceride levels significantly elevated in males because of increased VLDL triglycerides   (MGI Ref ID J:90737)
      • plasma triglyceride levels in females also tended to be elevated but not significantly   (MGI Ref ID J:90737)
      • heart content of triglycerides decreased   (MGI Ref ID J:90737)
      • postprandial levels tended to remain elevated   (MGI Ref ID J:90737)
  • cardiovascular system phenotype
  • abnormal cardiac cell glucose uptake
    • basal glucose uptake by the heart increased 8 fold   (MGI Ref ID J:90737)
    • tendency for insulin stimulated glucose uptake by the heart to increase somewhat   (MGI Ref ID J:90737)
  • muscle phenotype
  • abnormal cardiac cell glucose uptake
    • basal glucose uptake by the heart increased 8 fold   (MGI Ref ID J:90737)
    • tendency for insulin stimulated glucose uptake by the heart to increase somewhat   (MGI Ref ID J:90737)
  • cellular phenotype
  • abnormal cardiac cell glucose uptake
    • basal glucose uptake by the heart increased 8 fold   (MGI Ref ID J:90737)
    • tendency for insulin stimulated glucose uptake by the heart to increase somewhat   (MGI Ref ID J:90737)
View Research Applications

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

Cardiovascular Research
Hypertriglyceridemia
Other
      altered fat metabolism
      altered lipoprotein profile

Diabetes and Obesity Research
Hyperglycemia

Metabolism Research
Lipid Metabolism

Research Tools
Cardiovascular Research
      Cre-lox System
Cre-lox System
      loxP-flanked Sequences
Diabetes and Obesity Research
      loxP
Metabolism Research

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Lpltm1Ijg
Allele Name targeted mutation 1, Ira J Goldberg
Allele Type Targeted (Conditional ready (e.g. floxed), No functional change)
Common Name(s) Lpl loxP;
Mutation Made By Ira Goldberg,   Columbia University
Gene Symbol and Name Lpl, lipoprotein lipase
Chromosome 8
Gene Common Name(s) HDLCQ11; LIPD; O 1-4-5;
Molecular Note A single loxP site was introduced into intron 1 and a floxed neo was inserted upstream of exon 1. Transient cre excised the floxed neo, leaving floxed exon 1. Southern blot confirmed recombination and Northern blot demonstrated presence of RNA. [MGI Ref ID J:90737]

Genotyping

Genotyping Information

Genotyping Protocols

Lpltm1Ijg, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Augustus A; Yagyu H; Haemmerle G; Bensadoun A; Vikramadithyan RK; Park SY; Kim JK; Zechner R; Goldberg IJ. 2004. Cardiac-specific knock-out of lipoprotein lipase alters plasma lipoprotein triglyceride metabolism and cardiac gene expression. J Biol Chem 279(24):25050-7. [PubMed: 15028738]  [MGI Ref ID J:90737]

Additional References

Augustus AS; Buchanan J; Park TS; Hirata K; Noh HL; Sun J; Homma S; D'armiento J; Abel ED; Goldberg IJ. 2006. Loss of lipoprotein lipase-derived fatty acids leads to increased cardiac glucose metabolism and heart dysfunction. J Biol Chem 281(13):8716-23. [PubMed: 16410253]  [MGI Ref ID J:110484]

Pappan KL; Pan Z; Kwon G; Marshall CA; Coleman T; Goldberg IJ; McDaniel ML; Semenkovich CF. 2005. Pancreatic beta-cell lipoprotein lipase independently regulates islet glucose metabolism and normal insulin secretion. J Biol Chem 280(10):9023-9. [PubMed: 15637076]  [MGI Ref ID J:97791]

Lpltm1Ijg related

Augustus AS; Buchanan J; Park TS; Hirata K; Noh HL; Sun J; Homma S; D'armiento J; Abel ED; Goldberg IJ. 2006. Loss of lipoprotein lipase-derived fatty acids leads to increased cardiac glucose metabolism and heart dysfunction. J Biol Chem 281(13):8716-23. [PubMed: 16410253]  [MGI Ref ID J:110484]

Bharadwaj KG; Hiyama Y; Hu Y; Huggins LA; Ramakrishnan R; Abumrad NA; Shulman GI; Blaner WS; Goldberg IJ. 2010. Chylomicron- and VLDL-derived lipids enter the heart through different pathways: in vivo evidence for receptor- and non-receptor-mediated fatty acid uptake. J Biol Chem 285(49):37976-86. [PubMed: 20852327]  [MGI Ref ID J:167341]

Cano M; Fijalkowski N; Kondo N; Dike S; Handa J. 2011. Advanced Glycation Endproduct Changes to Bruch's Membrane Promotes Lipoprotein Retention by Lipoprotein Lipase. Am J Pathol 179(2):850-9. [PubMed: 21801873]  [MGI Ref ID J:174597]

Chen Y; Zhu J; Lum PY; Yang X; Pinto S; MacNeil DJ; Zhang C; Lamb J; Edwards S; Sieberts SK; Leonardson A; Castellini LW; Wang S; Champy MF; Zhang B; Emilsson V; Doss S; Ghazalpour A; Horvath S; Drake TA; Lusis AJ; Schadt EE. 2008. Variations in DNA elucidate molecular networks that cause disease. Nature 452(7186):429-35. [PubMed: 18344982]  [MGI Ref ID J:134171]

Duncan JG; Bharadwaj KG; Fong JL; Mitra R; Sambandam N; Courtois MR; Lavine KJ; Goldberg IJ; Kelly DP. 2010. Rescue of cardiomyopathy in peroxisome proliferator-activated receptor-alpha transgenic mice by deletion of lipoprotein lipase identifies sources of cardiac lipids and peroxisome proliferator-activated receptor-alpha activators. Circulation 121(3):426-35. [PubMed: 20065164]  [MGI Ref ID J:168445]

Garcia-Arcos I; Hiyama Y; Drosatos K; Bharadwaj KG; Hu Y; Son NH; O'Byrne SM; Chang CL; Deckelbaum RJ; Takahashi M; Westerterp M; Obunike JC; Jiang H; Yagyu H; Blaner WS; Goldberg IJ. 2013. Adipose-specific lipoprotein lipase deficiency more profoundly affects brown than white fat biology. J Biol Chem 288(20):14046-58. [PubMed: 23542081]  [MGI Ref ID J:198590]

Khan RS; Lin Y; Hu Y; Son NH; Bharadwaj KG; Palacios C; Chokshi A; Ji R; Yu S; Homma S; Schulze PC; Tian R; Goldberg IJ. 2013. Rescue of heart lipoprotein lipase-knockout mice confirms a role for triglyceride in optimal heart metabolism and function. Am J Physiol Endocrinol Metab 305(11):E1339-47. [PubMed: 24085031]  [MGI Ref ID J:204992]

Noh HL; Okajima K; Molkentin JD; Homma S; Goldberg IJ. 2006. Acute lipoprotein lipase deletion in adult mice leads to dyslipidemia and cardiac dysfunction. Am J Physiol Endocrinol Metab 291(4):E755-60. [PubMed: 16684851]  [MGI Ref ID J:127231]

Pappan KL; Pan Z; Kwon G; Marshall CA; Coleman T; Goldberg IJ; McDaniel ML; Semenkovich CF. 2005. Pancreatic beta-cell lipoprotein lipase independently regulates islet glucose metabolism and normal insulin secretion. J Biol Chem 280(10):9023-9. [PubMed: 15637076]  [MGI Ref ID J:97791]

Picard A; Rouch C; Kassis N; Moulle VS; Croizier S; Denis RG; Castel J; Coant N; Davis K; Clegg DJ; Benoit SC; Prevot V; Bouret S; Luquet S; Le Stunff H; Cruciani-Guglielmacci C; Magnan C. 2014. Hippocampal lipoprotein lipase regulates energy balance in rodents. Mol Metab 3(2):167-76. [PubMed: 24634821]  [MGI Ref ID J:208890]

Takahashi M; Yagyu H; Tazoe F; Nagashima S; Ohshiro T; Okada K; Osuga J; Goldberg IJ; Ishibashi S. 2013. Macrophage lipoprotein lipase modulates the development of atherosclerosis but not adiposity. J Lipid Res 54(4):1124-34. [PubMed: 23378601]  [MGI Ref ID J:195158]

Trent CM; Yu S; Hu Y; Skoller N; Huggins LA; Homma S; Goldberg IJ. 2014. Lipoprotein lipase activity is required for cardiac lipid droplet production. J Lipid Res 55(4):645-58. [PubMed: 24493834]  [MGI Ref ID J:208767]

Wang H; Astarita G; Taussig MD; Bharadwaj KG; DiPatrizio NV; Nave KA; Piomelli D; Goldberg IJ; Eckel RH. 2011. Deficiency of lipoprotein lipase in neurons modifies the regulation of energy balance and leads to obesity. Cell Metab 13(1):105-13. [PubMed: 21195353]  [MGI Ref ID J:169476]

Wang H; Knaub LA; Jensen DR; Young Jung D; Hong EG; Ko HJ; Coates AM; Goldberg IJ; de la Houssaye BA; Janssen RC; McCurdy CE; Rahman SM; Soo Choi C; Shulman GI; Kim JK; Friedman JE; Eckel RH. 2009. Skeletal muscle-specific deletion of lipoprotein lipase enhances insulin signaling in skeletal muscle but causes insulin resistance in liver and other tissues. Diabetes 58(1):116-24. [PubMed: 18952837]  [MGI Ref ID J:146987]

Yamashita H; Bharadwaj KG; Ikeda S; Park TS; Goldberg IJ. 2008. Cardiac metabolic compensation to hypertension requires lipoprotein lipase. Am J Physiol Endocrinol Metab 295(3):E705-13. [PubMed: 18647880]  [MGI Ref ID J:139973]

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 & HusbandryWhen maintaining a live colony, these mice are bred as homozygotes.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2140.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2782.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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