Strain Name:

B6 x BALB/cByJ-Lpin1fld/J

Stock Number:

002533

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Availability:

Cryopreserved - Ready for recovery

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 Mutant Strain; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse

Related Strains

Strains carrying   Lpin1fld allele
001592   BALB/cByJ-Lpin1fld/J
View Strains carrying   Lpin1fld     (1 strain)

Strains carrying other alleles of Lpin1
003401   C3H/HeJ-Lpin1fld-2J/J
012303   C57BL/6J-Lpin120884 Nrcam20884/Mmjax
View Strains carrying other alleles of Lpin1     (2 strains)

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.
Myoglobinuria, Acute Recurrent, Autosomal Recessive   (LPIN1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Lpin1fld/Lpin1fld

        BALB/cByJ-Lpin1fld/J
  • homeostasis/metabolism phenotype
  • abnormal enzyme/ coenzyme level
    • mRNA levels of phosphoenolpyruvate carboxykinase (PEPCK) and pyruvate carboxylase are significantly lower relative to wild-type; PEPCK expression is downregulated in response to feeding similar to wild-type, but pyruvate carboxylase levels do not change in mutants after feeding, indicating fatty acid synthesis is favored upon refeeding in mutants   (MGI Ref ID J:121022)
  • abnormal glucose homeostasis   (MGI Ref ID J:121022)
    • abnormal gluconeogenesis
      • fasting hepatic glucose production (HGP) is reduced by 43% relative to wild-type, indicating significant reduction in peripheral glucose uptake   (MGI Ref ID J:121022)
    • increased circulating glucose level
      • fasting plasma glucose levels are elevated (150 mg/dl) relative to wild-type (106 mg/dl)   (MGI Ref ID J:121022)
    • increased glycogen level
      • mutants have ~2-fold higher glycogen in liver and skeletal muscle as wild-type at 5 hours of re-feeding with normal chow after an 18 hour overnight fast   (MGI Ref ID J:121022)
      • this increase in glycogen content is not due to differences in food intake   (MGI Ref ID J:121022)
      • after 18 hour fast, liver glycogen content is reduced to ~4.5 mg/gram tissue in both wild-type and mutant, showing no significant difference   (MGI Ref ID J:121022)
  • abnormal metabolism
    • mutants display altered Cori cycle activity, as shown by significantly lower lactate production in response to 5 hours of refeeding; this contributes to the observed hepatic gluconeogenesis   (MGI Ref ID J:121022)
    • mutants have an overall reduction in flux through the Cori cycle   (MGI Ref ID J:121022)
  • abnormal respiratory quotient
    • during a 12 hour fast, the respiratory quotient (RQ) in wild-type mice drops from ~0.9 to 0.7, as shift from carbohydrate to primarily fatty acid metabolism by the end of the fast occurs, whereas in mutants, a decrease in RQ occurs but is considerably blunted   (MGI Ref ID J:121022)
    • homozygotes maintain significantly higher RQ than wild-type during the final 5 hours of the fast, indicating failure to rely on fatty acid fuels exclusively   (MGI Ref ID J:121022)
    • in contrast to wild-type, mutant RQ reaches its maximum value (0.85-0.89) at beginning of fasting and is only 0.83 at 5 hours of feeding; wild-type RQ increases to ~0.9 immediately upon feeding and remains relatively high until fasting begins   (MGI Ref ID J:121022)
  • increased fatty acid level
    • mutants show increased hepatic fatty acid synthesis compared to wild-type mice   (MGI Ref ID J:121022)
    • fatty acid synthesis rate for mutants is 0.27 vs 0.063 in wild-type   (MGI Ref ID J:121022)
  • nervous system phenotype
  • abnormal action potential
    • reduced motor nerve conduction velocity is accompanied by temporal dispersion and reduction of compound muscle action potentials   (MGI Ref ID J:137213)
  • abnormal myelination
    • delay in myelination apparent in the sciatic nerve by P10   (MGI Ref ID J:137213)
    • at P56 no normally myelinated axons are present in the sciatic nerve   (MGI Ref ID J:137213)
  • abnormal sciatic nerve morphology
    • dramatic reduction in the number of adipocytes in the epineurium   (MGI Ref ID J:137213)
    • massive accumulation of lipid droplets in the perineurial and endoneurial compartments   (MGI Ref ID J:137213)
  • decreased nerve conduction velocity
    • strong reduction in motor nerve conduction velocity of the sciatic nerve at P56   (MGI Ref ID J:137213)
  • behavior/neurological phenotype
  • limb grasping
    • clench toes of the hind feet when lifted by the tail   (MGI Ref ID J:137213)

Lpin1fld/Lpin1fld

        BALB/cByJ-Lpin1fld
  • mortality/aging
  • decreased survivor rate   (MGI Ref ID J:9801)
  • partial lethality at weaning
    • the majority of mice fail to make the transition to grain   (MGI Ref ID J:9801)
  • partial postnatal lethality
    • some mice die before weaning   (MGI Ref ID J:82882)
  • premature death
    • many mice die between 19 and 35 days after birth   (MGI Ref ID J:82882)
  • growth/size/body phenotype
  • decreased body weight
    • by third day after birth, mice display significantly reduced weigh gain, and remain 25-30% underweight throughout their lifetime   (MGI Ref ID J:63448)
  • decreased lean body mass
    • may be reduced, as body weight is reduced 25-30% and adipose tissue is ~15% of body weight   (MGI Ref ID J:63448)
  • distended abdomen
    • by P3, mutants can be identified by their distended abdomens   (MGI Ref ID J:82882)
  • behavior/neurological phenotype
  • abnormal gait
    • homoyzgotes develop an unsteady gait starting at ~P10, and this persists throughout life   (MGI Ref ID J:82882)
  • abnormal motor coordination/ balance   (MGI Ref ID J:9801)
    • impaired limb coordination
      • adults lack hind limb coordination   (MGI Ref ID J:9801)
  • limb grasping
    • when lifted by the tail, mice clench toes of the hind feet and clasp hind limbs together   (MGI Ref ID J:82882)
  • tremors
    • mice display generalized tremors starting ~P10   (MGI Ref ID J:82882)
  • nervous system phenotype
  • abnormal PNS glial cell morphology   (MGI Ref ID J:82882)
    • abnormal Schwann cell morphology
      • numerous hypertrophic cells with increased nuclear size, abnormally large mitochondria and copius cytoplasm are observed, and some cells contain myelin degradation debris; this becomes more widely distributed by 30 days and persist through 1 year   (MGI Ref ID J:82882)
      • abnormal cells are more common in older mice   (MGI Ref ID J:82882)
      • in adults, free cell processes and basal lamina are frequently found, but onion bulb formation is rare   (MGI Ref ID J:82882)
  • abnormal axon morphology   (MGI Ref ID J:82882)
    • abnormal myelin sheath morphology
      • sheaths around axons of the sciatic nerve at postnatal day 4 are markedly thin compared to controls; this persists through 1 year of age   (MGI Ref ID J:82882)
  • abnormal sciatic nerve morphology
    • axonal myelin sheaths are thin, hypertrophic Schwann cells are observed, sometimes accumulating myelin debris with age   (MGI Ref ID J:82882)
  • axon degeneration
    • in adult sciatic nerves, some degenerating axons are observed, along with bands of Bugner, and regenerative clusters occasionally   (MGI Ref ID J:82882)
  • reproductive system phenotype
  • delayed female fertility
    • females do not generally produce their first litter until ~90 days of age   (MGI Ref ID J:82882)
  • female infertility
    • ~50% of females are infertile   (MGI Ref ID J:82882)
  • male infertility
    • all males appear to be infertile, possibly due to behavior impairment   (MGI Ref ID J:82882)
  • adipose tissue phenotype
  • abnormal brown adipose tissue morphology
    • in adults and neonates, tissue appears abnormal   (MGI Ref ID J:63448)
    • brown adipose tissue sections at 1 and 6 months of age exhibit dramatically reduced lipid content relative to controls; in some regions, tissue consists largely of muscle with small masses of lipid-poor adipocytes   (MGI Ref ID J:63448)
    • decreased brown adipose tissue amount   (MGI Ref ID J:66739)
      • mice exhibit reduced fat mass in brown adipose tissue depots   (MGI Ref ID J:63448)
      • interscapular brown adipose tissue mass is reduced 80% in adults, but not in neonates   (MGI Ref ID J:63448)
    • decreased brown fat cell lipid droplet size   (MGI Ref ID J:66739)
  • abnormal brown adipose tissue physiology
    • brown adipose tissue levels of uncoupling protein 1 mRNA are reduced   (MGI Ref ID J:63448)
    • PPARgamma and adipocyte fatty acid-binding protein aP2 mRNA levels are markedly elevated in mutants, most evident at 2 weeks of age and less pronounced in older mice   (MGI Ref ID J:63448)
  • abnormal epididymal fat pad morphology
    • epididymal fat pads from 1-month old mice have immature cells containing mostly small, sparse lipid droplets   (MGI Ref ID J:63448)
    • decreased epididymal fat pad weight
      • epididymal fat pad mass is reduced ~80% in neonates and adults   (MGI Ref ID J:63448)
  • abnormal fat cell morphology
    • at 1 and 6 months of age, adipocytes are found to be severely depleted of lipid   (MGI Ref ID J:63448)
    • by 6 months, white adipocytes have accumulated more lipid than at 1 month, but cells remain reduced in size and contain a heterogeneous population of lipid droplets characteristic of incompletely differentiated adipocytes   (MGI Ref ID J:63448)
    • in some regions of brown adipose tissue sections at 1 and 6 months of age, tissue consists largely of muscle with small masses of lipid-poor adipocytes   (MGI Ref ID J:63448)
    • adipocytes appear immature with sparse lipid droplets   (MGI Ref ID J:66739)
    • decreased brown fat cell lipid droplet size   (MGI Ref ID J:66739)
    • decreased white fat cell lipid droplet size   (MGI Ref ID J:66739)
  • abnormal white adipose tissue physiology
    • white adipose tissue expresses reduced mRNA levels of lipoprotein lipase, as well as adipsin and uncoupling protein 1   (MGI Ref ID J:63448)
    • after weaning, expression of fatty acid synthase and acetyl-CoA carboxylase is relatively unchanged compared to wild-type where expression is highly induced   (MGI Ref ID J:63448)
  • decreased inguinal fat pad weight
    • fat pad mass is reduced ~80% in neonates and adults   (MGI Ref ID J:63448)
  • decreased interscapular fat pad weight
    • interscapular brown adipose tissue mass is reduced 80% in adults, but not in neonates   (MGI Ref ID J:63448)
  • decreased white adipose tissue amount   (MGI Ref ID J:66739)
    • mice exhibit reduced fat mass in white adipose tissue depots   (MGI Ref ID J:63448)
  • cardiovascular system phenotype
  • abnormal aorta morphology
    • after 16 weeks of an atherogenic diet, mutants display 2-fold greater lesion area relative to wild-type littermates; lesions are qualitatively more advanced than in wild-type   (MGI Ref ID J:63448)
    • lesions extend beyond aortic valve attachment points to form raised lesions in the free aortic wall   (MGI Ref ID J:63448)
    • raised lesions are detected in 92% of homozygotes vs only 44% of wild-type mice   (MGI Ref ID J:63448)
  • homeostasis/metabolism phenotype
  • abnormal enzyme/coenzyme activity   (MGI Ref ID J:82882)
    • decreased hormone-sensitive lipase activity
      • in 3-week old mice, hormone-sensitive lipase activity is reduced ~50% compared to wild-type tissue (29 vs 60 mU/mg)   (MGI Ref ID J:63448)
    • decreased lipoprotein lipase activity
      • during the suckling period, lipoprotein lipase activity is reduced by ~16-fold in white adipose tissue and by <2-fold in the heart of mutants   (MGI Ref ID J:82882)
    • decreased triglyceride lipase activity
      • hepatic lipase activity and mRNA levels are reduced ~6-fold and 2-fold respectively compared to wild-type: abnormalities resolve between 14 and 28 days postnatal   (MGI Ref ID J:82882)
  • abnormal lipid homeostasis
    • sphingomyelin and galactosphingolipids and sulfatides exhibit age-dependent decreases in levels relative to phosphotidylcholine in mutants but not in wild-type   (MGI Ref ID J:82882)
    • abnormal cholesterol homeostasis
      • mice have increased cholesterol ester levels in sciatic nerve extracts at 1-2 and 3+ months of age relative to wild-type   (MGI Ref ID J:82882)
      • decreased circulating LDL cholesterol level
        • on an atherogenic diet, the LDL/VLDL fraction (60%) makes up less of the total cholesterol compared to wild-type (76%)   (MGI Ref ID J:63448)
      • decreased circulating VLDL cholesterol level
        • on an atherogenic diet for 16 weeks, the LDL/VLDL fraction (60%) makes up less of the total cholesterol compared to wild-type (76%)   (MGI Ref ID J:63448)
      • increased cholesterol level
        • levels are significantly less in sciatic nerve lipids (552, 226 ng/ug) vs wild-type (896, 526 ng/ug) at 1-2 months and 3+ months respectively   (MGI Ref ID J:82882)
        • increased circulating HDL cholesterol level
          • on an atherogenic diet for 16 weeks, the HDL fraction (40% of total) accounts for more cholesterol than in wild-type (24%)   (MGI Ref ID J:63448)
    • abnormal lipid level
      • within several days of birth, hepatic levels of apolipoprotein ApoA-IV mRNA are increased 100-fold and ApoC-II mRNA levels are 6-fold increased relative to wild-type   (MGI Ref ID J:82882)
      • abnormal phospholipid level
        • at 3 months of age, sciatic nerve lipids show an elevation of neutral lipid species and alteration of relative amounts of phosphatidylserine, phophatidyl- or phophatidalethanolamine, phophatidylcholine, and sphingomyelin compared to control levels   (MGI Ref ID J:82882)
        • phosphotidylinositol:phosphotidylcholine ratio is slightly increased in mutant nerves relative to wild-type   (MGI Ref ID J:82882)
        • lipid profile resembles that of an immature nerve or one undergoing repair   (MGI Ref ID J:82882)
        • at 3+ months of age, phosphatidylcholine levels in sciatic nerve extracts are 3.3 times the level in wild-type, while levels of phosphatidal- and phosphotidylethanolamines and phosphotidalserine are lower than controls at all ages, and difference from wild type increases with age   (MGI Ref ID J:82882)
      • abnormal triglyceride level   (MGI Ref ID J:82882)
        • decreased triglyceride level
          • at 3+ months, ratio of triglycerides to cholesterol in sciatic nerves is slightly lower than wild-type   (MGI Ref ID J:82882)
        • increased triglyceride level   (MGI Ref ID J:82882)
          • increased circulating triglyceride level
            • within a few days after birth, serum triglyceride levels are elevated by several fold relative to controls   (MGI Ref ID J:82882)
            • increased circulating VLDL triglyceride level
              • adult hepatocytes secrete more VLDL-sized apoB48-containing particles than do hepatocytes from littermate controls, and hepatic overexpression of lipin 1 markedly suppresses triglyceride secretion resulting in less VLDL-sized particles and more HDL-like particles   (MGI Ref ID J:147417)
          • increased liver triglyceride level
            • within a few days after birth, hepatic triglyceride levels are elevated by several fold relative to controls   (MGI Ref ID J:82882)
            • hepatocytes isolated from 14 day old homozygotes have significantly increased triglyceride synthesis and secretion rates   (MGI Ref ID J:147417)
            • hepatoctyes isolated from 42 day old adult homozygotes have normal synthesis but increased secretion of triglycerides   (MGI Ref ID J:147417)
      • decreased circulating LDL cholesterol level
        • on an atherogenic diet, the LDL/VLDL fraction (60%) makes up less of the total cholesterol compared to wild-type (76%)   (MGI Ref ID J:63448)
      • decreased circulating VLDL cholesterol level
        • on an atherogenic diet for 16 weeks, the LDL/VLDL fraction (60%) makes up less of the total cholesterol compared to wild-type (76%)   (MGI Ref ID J:63448)
      • decreased fatty acid level
        • in response to atherogenic diet, mutants have slightly lower fatty acid levels than wild-type   (MGI Ref ID J:63448)
      • increased cholesterol level
        • levels are significantly less in sciatic nerve lipids (552, 226 ng/ug) vs wild-type (896, 526 ng/ug) at 1-2 months and 3+ months respectively   (MGI Ref ID J:82882)
        • increased circulating HDL cholesterol level
          • on an atherogenic diet for 16 weeks, the HDL fraction (40% of total) accounts for more cholesterol than in wild-type (24%)   (MGI Ref ID J:63448)
      • increased fatty acid level
        • levels in sciatic nerve extracts are 2-fold higher than wild-type at 3+ months of age   (MGI Ref ID J:82882)
  • decreased circulating leptin level
    • plasma leptin levels are significantly reduced   (MGI Ref ID J:66739)
  • decreased insulin secretion
    • 60 minutes following glucose injection, mutant insulin levels are slightly higher than in wild-type but lower than that measured in non-glucose-challenged mutants indicating impaired secretion   (MGI Ref ID J:63448)
  • impaired glucose tolerance
    • mice have impaired clearance of a glucose dose with levels remaining >400 mg/dl for 2 hours after glucose administration, in contrast to levels in wild-type mice which return to baseline after 1 hour   (MGI Ref ID J:63448)
  • increased circulating insulin level
    • nonfasting insulin levels are elevated 2.5-fold in mutants on a regular chow diet   (MGI Ref ID J:63448)
    • on an atherogenic diet for 16 weeks, insulin levels in plasma are reduced in mutants and wild-type, but levels in mutant mice are 4-fold higher than in wild-type   (MGI Ref ID J:63448)
  • insulin resistance
    • administration of exogenous insulin with glucose injection does not produce the typical hypoglycemic response seen in wild-type   (MGI Ref ID J:63448)
  • liver/biliary system phenotype
  • enlarged liver
    • homozygotes can be recognized as early as P3 by their large livers   (MGI Ref ID J:82882)
    • liver is 2-fold larger than wild-type in neonates, and 20% larger in adults   (MGI Ref ID J:63448)
  • increased liver triglyceride level
    • within a few days after birth, hepatic triglyceride levels are elevated by several fold relative to controls   (MGI Ref ID J:82882)
    • hepatocytes isolated from 14 day old homozygotes have significantly increased triglyceride synthesis and secretion rates   (MGI Ref ID J:147417)
    • hepatoctyes isolated from 42 day old adult homozygotes have normal synthesis but increased secretion of triglycerides   (MGI Ref ID J:147417)
  • pale liver
    • homozygotes can be recognized as early as P3 by their pale livers   (MGI Ref ID J:82882)
  • endocrine/exocrine gland phenotype
  • decreased insulin secretion
    • 60 minutes following glucose injection, mutant insulin levels are slightly higher than in wild-type but lower than that measured in non-glucose-challenged mutants indicating impaired secretion   (MGI Ref ID J:63448)
  • integument phenotype
  • abnormal hair growth
    • ruffled coat appearance is due to reduced hair growth   (MGI Ref ID J:82882)
    • retarded hair growth   (MGI Ref ID J:9801)
  • disheveled coat
    • mice have unkempt coat appearance   (MGI Ref ID J:82882)
  • ruffled hair
    • mice have coats with ruffled appearance   (MGI Ref ID J:82882)

Lpin1fld/Lpin1fld

        involves: BALB/cByJ
  • reproductive system phenotype
  • abnormal spermatocyte morphology
    • nuage (intermitochondrial cement) between mitochondria is increased in density and longer compared to wild-type spermatocytes   (MGI Ref ID J:169933)
View Research Applications

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

Lpin1fld related

Developmental Biology Research
Internal/Organ Defects
      liver

Internal/Organ Research
Liver Defects

Metabolism Research

Neurobiology Research
Ataxia (Movement) Defects
Metabolic Defects
Myelination Defects
      peripheral neuropathy
Tremor Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Lpin1fld
Allele Name fatty liver dystrophy
Allele Type Spontaneous
Common Name(s) fld;
Strain of OriginBALB/cByJ
Gene Symbol and Name Lpin1, lipin 1
Chromosome 12
Gene Common Name(s) Lipin1; PAP1; fatty liver dystrophy; fld; mKIAA0188;
Molecular Note Three molecular changes have been identified in this allele. A 2 kb deletion encompasses exons 2 and 3 including the translation initiation sequence. An inversion exceeding 40 kb encompasses much of the coding region. An additional 0.5 kb sequence downstream of the inverted 40 kb has been duplicated and inserted in reverse orientation just upstream of this 40 kb inversion. Northern blots of adipose tissue extracts failed to detect mRNA from mice homozygous for this allele. [MGI Ref ID J:66739]

Genotyping

Genotyping Information


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Lpin1fld related

Chen Z; Gropler MC; Norris J; Lawrence JC Jr; Harris TE; Finck BN. 2008. Alterations in hepatic metabolism in fld mice reveal a role for lipin 1 in regulating VLDL-triacylglyceride secretion. Arterioscler Thromb Vasc Biol 28(10):1738-44. [PubMed: 18669885]  [MGI Ref ID J:147417]

Donkor J; Sariahmetoglu M; Dewald J; Brindley DN; Reue K. 2007. Three mammalian lipins act as phosphatidate phosphatases with distinct tissue expression patterns. J Biol Chem 282(6):3450-7. [PubMed: 17158099]  [MGI Ref ID J:120935]

Douglas DS; Moran JL; Bermingham JR Jr; Chen XJ; Brindley DN; Soliven B; Beier DR; Popko B. 2009. Concurrent Lpin1 and Nrcam mouse mutations result in severe peripheral neuropathy with transitory hindlimb paralysis. J Neurosci 29(39):12089-100. [PubMed: 19793967]  [MGI Ref ID J:153042]

Finck BN; Gropler MC; Chen Z; Leone TC; Croce MA; Harris TE; Lawrence JC Jr; Kelly DP. 2006. Lipin 1 is an inducible amplifier of the hepatic PGC-1alpha/PPARalpha regulatory pathway. Cell Metab 4(3):199-210. [PubMed: 16950137]  [MGI Ref ID J:129744]

Gazit V; Weymann A; Hartman E; Finck BN; Hruz PW; Tzekov A; Rudnick DA. 2010. Liver regeneration is impaired in lipodystrophic fatty liver dystrophy mice. Hepatology 52(6):2109-17. [PubMed: 20967828]  [MGI Ref ID J:204049]

Gropler MC; Harris TE; Hall AM; Wolins NE; Gross RW; Han X; Chen Z; Finck BN. 2009. Lipin 2 is a liver-enriched phosphatidate phosphohydrolase enzyme that is dynamically regulated by fasting and obesity in mice. J Biol Chem 284(11):6763-72. [PubMed: 19136718]  [MGI Ref ID J:148371]

Hall AM; Brunt EM; Chen Z; Viswakarma N; Reddy JK; Wolins NE; Finck BN. 2010. Dynamic and differential regulation of proteins that coat lipid droplets in fatty liver dystrophic mice. J Lipid Res 51(3):554-63. [PubMed: 19749180]  [MGI Ref ID J:159055]

Huang H; Gao Q; Peng X; Choi SY; Sarma K; Ren H; Morris AJ; Frohman MA. 2011. piRNA-Associated Germline Nuage Formation and Spermatogenesis Require MitoPLD Profusogenic Mitochondrial-Surface Lipid Signaling. Dev Cell 20(3):376-87. [PubMed: 21397848]  [MGI Ref ID J:169933]

Klingenspor M; Xu P; Cohen RD; Welch C; Reue K. 1999. Altered gene expression pattern in the fatty liver dystrophy mouse reveals impaired insulin-mediated cytoskeleton dynamics. J Biol Chem 274(33):23078-84. [PubMed: 10438476]  [MGI Ref ID J:42314]

Kok BP; Kienesberger PC; Dyck JR; Brindley DN. 2012. Relationship of glucose and oleate metabolism to cardiac function in lipin-1 deficient (fld) mice. J Lipid Res 53(1):105-18. [PubMed: 22058427]  [MGI Ref ID J:179394]

Langner CA; Birkenmeier EH; Ben-Zeev O; Schotz MC; Sweet HO; Davisson MT; Gordon JI. 1989. The fatty liver dystrophy (fld) mutation. A new mutant mouse with a developmental abnormality in triglyceride metabolism and associated tissue-specific defects in lipoprotein lipase and hepatic lipase activities. J Biol Chem 264(14):7994-8003. [PubMed: 2722772]  [MGI Ref ID J:9801]

Langner CA; Birkenmeier EH; Roth KA; Bronson RT; Gordon JI. 1991. Characterization of the peripheral neuropathy in neonatal and adult mice that are homozygous for the fatty liver dystrophy (fld) mutation. J Biol Chem 266(18):11955-64. [PubMed: 2050689]  [MGI Ref ID J:82882]

Nadra K; Charles AS; Medard JJ; Hendriks WT; Han GS; Gres S; Carman GM; Saulnier-Blache JS; Verheijen MH; Chrast R. 2008. Phosphatidic acid mediates demyelination in Lpin1 mutant mice. Genes Dev 22(12):1647-61. [PubMed: 18559480]  [MGI Ref ID J:137213]

Nadra K; Medard JJ; Quignodon L; Verheijen MH; Desvergne B; Chrast R. 2012. Epineurial adipocytes are dispensable for Schwann cell myelination. J Neurochem 123(5):662-7. [PubMed: 22849425]  [MGI Ref ID J:190578]

Peterfy M; Phan J; Xu P; Reue K. 2001. Lipodystrophy in the fld mouse results from mutation of a new gene encoding a nuclear protein, lipin Nat Genet 27(1):121-4. [PubMed: 11138012]  [MGI Ref ID J:66739]

Phan J; Peterfy M; Reue K. 2004. Lipin expression preceding peroxisome proliferator-activated receptor-gamma is critical for adipogenesis in vivo and in vitro. J Biol Chem 279(28):29558-64. [PubMed: 15123608]  [MGI Ref ID J:91675]

Phan J; Reue K. 2005. Lipin, a lipodystrophy and obesity gene. Cell Metab 1(1):73-83. [PubMed: 16054046]  [MGI Ref ID J:129850]

Rehnmark S; Giometti CS; Slavin BG; Doolittle MH; Reue K. 1998. The fatty liver dystrophy mutant mouse: microvesicular steatosis associated with altered expression levels of peroxisome proliferator-regulated proteins. J Lipid Res 39(11):2209-17. [PubMed: 9799807]  [MGI Ref ID J:50756]

Ren H; Federico L; Huang H; Sunkara M; Drennan T; Frohman MA; Smyth SS; Morris AJ. 2010. A phosphatidic acid binding/nuclear localization motif determines lipin1 function in lipid metabolism and adipogenesis. Mol Biol Cell 21(18):3171-81. [PubMed: 20660155]  [MGI Ref ID J:182849]

Reue K; Brindley DN. 2008. Thematic Review Series: Glycerolipids. Multiple roles for lipins/phosphatidate phosphatase enzymes in lipid metabolism. J Lipid Res 49(12):2493-503. [PubMed: 18791037]  [MGI Ref ID J:143110]

Reue K; Doolittle MH. 1996. Naturally occurring mutations in mice affecting lipid transport and metabolism. J Lipid Res 37(7):1387-405. [PubMed: 8827513]  [MGI Ref ID J:34179]

Reue K; Xu P; Wang XP; Slavin BG. 2000. Adipose tissue deficiency, glucose intolerance, and increased atherosclerosis result from mutation in the mouse fatty liver dystrophy (fld) gene J Lipid Res 41(7):1067-76. [PubMed: 10884287]  [MGI Ref ID J:63448]

Shin J; Zhang P; Wang S; Wu J; Guan Z; Zhong XP. 2013. Negative control of mast cell degranulation and the anaphylactic response by the phosphatase lipin1. Eur J Immunol 43(1):240-8. [PubMed: 23065777]  [MGI Ref ID J:191099]

Sweet HO; Birkenmeier E; Davisson MT. 1988. fld - fatty liver dystrophy Mouse News Lett 81:69.  [MGI Ref ID J:64452]

Verheijen MH; Chrast R; Burrola P; Lemke G. 2003. Local regulation of fat metabolism in peripheral nerves. Genes Dev 17(19):2450-64. [PubMed: 14522948]  [MGI Ref ID J:90859]

Xu J; Lee WN; Phan J; Saad MF; Reue K; Kurland IJ. 2006. Lipin deficiency impairs diurnal metabolic fuel switching. Diabetes 55(12):3429-38. [PubMed: 17130489]  [MGI Ref ID J:121022]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

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

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* $3300.00
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 willfulfill 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* $4290.00
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 willfulfill 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.

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.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

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.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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