Strain Name:

BKS.Cg-Dock7m +/+ Leprdb/J

Stock Number:

000642

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Availability:

Level 2

Mice homozygous for the diabetes spontaneous mutation (Leprdb) become obese at approximately three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days and elevations of blood sugar at four to eight weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The severity of disease on this genetic background leads to an uncontrolled rise in blood sugar, severe depletion of the insulin-producing beta-cells of the pancreatic islets, and death by 10 months of age. Exogenous insulin fails to control blood glucose levels and gluconeogenic enzyme activity increases. Peripheral neuropathy and myocardial disease are seen in C57BLKS-Leprdb homozygotes. Wound healing is delayed, and metabolic efficiency is increased.

Description

Strain Information

Former Names BKS.Cg-m +/+ Leprdb/J    (Changed: 28-APR-09 )
BKS.Cg-m+/+Leprdb/J    (Changed: 25-JAN-07 )
C57BLKS-m Leprdb    (Changed: 17-NOV-05 )
Type Coisogenic; Congenic; Mutant Strain; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Breeding Considerations This strain is a good breeder.
Specieslaboratory mouse
Background Strain C57BLKS/J
Donor Strain Leprdb, C57BLKS; Dock7m, DBA/J
H2 Haplotyped
GenerationF131 (05-AUG-14)
Generation Definitions

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Appearance
Leprdb: black, fat
Related Genotype: a/a + Leprdb/+ Leprdb

Dock7m Leprdb: black, lean
Related Genotype: a/a Dock7m +/+ Leprdb

Dock7m: misty (grey), lean
Related Genotype: a/a Dock7m +/Dock7m +

Important Note
This strain is maintained with Dock7m and Leprdb in repulsion. Although these genes are tightly linked, there is a small possibility of recombination. The heterozygotes we distribute are presumed to be non-recombinant, but are untested.

Description
Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days of age and of blood sugar at four to eight weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. A number of features are observed on the C57BLKS background, including an uncontrolled rise in blood sugar, severe depletion of the insulin-producing beta-cells of the pancreatic islets, and death by 10 months of age. Exogenous insulin fails to control blood glucose levels and gluconeogenic enzyme activity increases. Peripheral neuropathy and myocardial disease are seen in C57BLKS-Leprdb homozygotes. Wound healing is delayed, and metabolic efficiency is increased. Female homozygotes exhibit decreased uterine and ovarian weights, decreased ovarian hormone production and hypercytolipidemia in follicular granulosa and endometrial epithelial tissue layers (Garris et al., 2004, Garris et al., 2004).

Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Leprdb/+) also have increased metabolic efficiency and can survive a prolonged fast longer than controls. Experiments involving destruction of the ventromedial nucleus of the hypothalamus suggest that Leprdb may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in diabetic mice, interact with the Leprdb mutation as modifiers of gender differences in obesity-induced diabetes susceptibility. Because of the sterility of Leprdb homozygotes, the misty (Dock7m) mutation has been incorporated into stocks for maintenance of the diabetes mutation. The repulsion double heterozygote (Dock7m +/+ Leprdb) facilitates identification of heterozygotes for breeding, while the coupling double heterozygote, (Dock7m Leprdb/+ +) allows identification of homozygotes before the onset of clinical symptoms.

The recessive misty mutation causes a mild dilution of coat color and on certain backgrounds a white tail tip often accompanied by a belly spot. Melanocytes from Dock7m/Dock7m mice have a highly dendritic shape, show deficient proliferation in culture and have much more melanin content. Fewer melanoblasts are found in primary cultures from Dock7m/Dock7m mice than from wildtype controls. Between two and five weeks of age, Dock7m/Dock7m mice are smaller than controls. At 35 days of age they are shorter, weigh 15% less on average, and have less inguinal adipose mass than controls. Misty homozygotes completely lack brown fat. Although platelet count, seratonin content and ATP content are normal, Dock7m/Dock7m homozygotes have an increased bleed time and reduced platelet ADP levels.(Woolley 1941 and 1945; Truett et al. 1998; Sviderskaya et al. 1998.)

Control Information

  Control
   Dock7m +/+ Leprdb (Heterozygote from the colony)
   Dock7m +/Dock7m + from the colony
   000662 C57BLKS/J
 
  Considerations for Choosing Controls

Related Strains

View Strains carrying   Dock7m     (8 strains)

View Strains carrying   Leprdb     (9 strains)

Strains carrying other alleles of Lepr
000709   129P3/J-Leprdb-3J/J
017527   B6.129(FVB)-Leprtm5Mgmj/J
008518   B6.129-Leprtm1Mgmj/J
008320   B6.129-Leprtm2(cre)Rck/J
008385   B6.129-Leprtm2Mgmj/J
008327   B6.129P2-Leprtm1Rck/J
004939   NOD/ShiLtJ-Leprdb-5J/LtJ
006846   STOCK Leprdb-9J/Jgn
018989   STOCK Leprtm1Jke/J
View Strains carrying other alleles of Lepr     (9 strains)

Additional Web Information

Comparison of widely used JAX® Mice for type 2 diabetes and obesity
JAX® NOTES, Spring 2003; 489. Malocclusion in the Laboratory Mouse.
JAX® NOTES, Summer 2003; 490. Hydrocephalus in Laboratory Mice.
JAX® NOTES, Summer 2008; 510. BKS.Cg-m +/+ Leprdb/J (000642), One of the Most Widely-used Diabetes Models at JAX
JAX® NOTES, Summer 2009; 514. Restoring Leptin Signaling in Key Neurons Normalizes Metabolism.

Phenotype

Phenotype Information

View Phenotypic Data

Phenotypic Data
Mouse Phenome Database
View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Diabetes Mellitus, Noninsulin-Dependent; NIDDM
Obesity
Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.
Storage Pool Platelet Disease
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Leptin Receptor Deficiency   (LEPR)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Dock7m/Dock7m

        BKS.Cg-Dock7m +/+ Leprdb/BomTac
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • homozygous mutant and wild type control (C57BL/6J) mice exhibit similar locomotor activity; response in the tail-suspension test for depressive behavior; learning as measured by habituation of object exploration; working memory as measured using the Y maze; anxiety-like behavior in a light-dark transfer test; and preference for social familiarity/novelty   (MGI Ref ID J:146458)

Leprdb/Lepr+

        involves: C57BLKS/J
  • homeostasis/metabolism phenotype
  • abnormal glucose homeostasis   (MGI Ref ID J:71934)
    • abnormal circulating insulin level
      • 2.2X increase in fasting insulin during pregnancy compared to a 3X increase in controls   (MGI Ref ID J:71934)
      • leptin treatment results in a 14% reduction in insulin levels compared to a 45% reduction in controls   (MGI Ref ID J:71934)
    • impaired glucose tolerance
      • profound glucose intolerance during pregnancy   (MGI Ref ID J:71934)
      • glucose levels 41% higher in a glucose tolerance test at 30 and at 60 minute time points   (MGI Ref ID J:71934)
      • 45-55% higher glucose levels after a glucose challenge but dramatically improved by leptin treatment and glucose levels reduced 33 and 30% in glucose tolerance tests at 30 and 60 minute time points   (MGI Ref ID J:71934)
    • increased circulating glucose level
      • fasting glucose levels elevated 25% during pregnancy   (MGI Ref ID J:71934)
  • abnormal hormone level
    • elevated placental leptin levels in pregnant females   (MGI Ref ID J:71934)
    • abnormal circulating insulin level
      • 2.2X increase in fasting insulin during pregnancy compared to a 3X increase in controls   (MGI Ref ID J:71934)
      • leptin treatment results in a 14% reduction in insulin levels compared to a 45% reduction in controls   (MGI Ref ID J:71934)
  • behavior/neurological phenotype
  • increased food intake
    • food intake 11% greater than controls during pregnancy   (MGI Ref ID J:71934)
    • leptin treatment suppresses food intake to near control levels   (MGI Ref ID J:71934)
  • growth/size/body phenotype
  • increased susceptibility to weight gain
    • 33% greater maternal weight gain   (MGI Ref ID J:71934)
    • maternal body weight at term 24% greater than controls   (MGI Ref ID J:71934)
    • birth weights significantly heavier than controls and unaffected by maternal leptin treatment unlike controls where maternal leptin treatment causes a decrease in birth weights   (MGI Ref ID J:71934)
  • increased total body fat amount
    • 20% greater adipose tissue mass during pregnancy than in controls   (MGI Ref ID J:71934)
  • adipose tissue phenotype
  • increased total body fat amount
    • 20% greater adipose tissue mass during pregnancy than in controls   (MGI Ref ID J:71934)

Leprdb/Lepr+

        BKS.Cg-Dock7m +/+ Leprdb/J
  • mortality/aging
  • extended life span
    • increased survival when totally deprived of food than wild-type controls   (MGI Ref ID J:6081)
    • survival when deprived of food is longer rhan when in a C57BL/6 background   (MGI Ref ID J:6081)

Leprdb/Leprdb

        involves: C57BLKS/J
  • homeostasis/metabolism phenotype
  • abnormal glucose homeostasis   (MGI Ref ID J:80996)
    • decreased circulating glucose level
      • mice treated with adenovirus expressing Adipor1 (1.5-fold increase in liver expression), show decreased plasma glucose compared to wild-type   (MGI Ref ID J:117919)
      • mice treated with an adenovirus expressing Adipor2 (5-fold increase in liver expression), show decreased plasma glucose compared to wild-type   (MGI Ref ID J:117919)
    • decreased circulating insulin level
      • mice treated with an adenovirus expressing Adipor 2 show improved glucose resistance and decreased plasma insulin level   (MGI Ref ID J:117919)
    • impaired glucose tolerance   (MGI Ref ID J:89242)
    • increased circulating glucose level   (MGI Ref ID J:5010)
      • plasma fasting glucose is increased   (MGI Ref ID J:89242)
      • hyperglycemia
        • diabetes is improved after treatment with an adenovirus expressing Adipor1 or Adipor2   (MGI Ref ID J:117919)
    • increased circulating insulin level   (MGI Ref ID J:5010)
      • fasting insulin is increased   (MGI Ref ID J:89242)
    • insulin resistance
      • mice treated with an adenovirus expressing Adipor1 or Adipor 2 show improved insulin resistance   (MGI Ref ID J:117919)
  • abnormal vascular wound healing
    • reduced neointimal area relative to controls 4 weeks after femoral artery injury   (MGI Ref ID J:135034)
    • vascular smooth muscle proliferation significantly reduced   (MGI Ref ID J:135034)
  • impaired adaptive thermogenesis
    • mutants become hypothermic after a 12 hour fast   (MGI Ref ID J:89242)
    • mutants housed at 4 degrees C for 3.5 hours cannot maintain their body temperature like wild-type and drop about 1 degree in body temperature every 30 min until they reach 34 degrees C, at which point they stabilize this temperature, indicating decreased sympathetic activity   (MGI Ref ID J:89242)
  • increased circulating corticosterone level   (MGI Ref ID J:89242)
  • increased circulating leptin level   (MGI Ref ID J:89242)
  • increased urine protein level
    • in females when compared to female controls   (MGI Ref ID J:5257)
    • levels of protein in urine similar in males and females but levels in males lower than in male controls   (MGI Ref ID J:5257)
  • growth/size/body phenotype
  • decreased body length
    • mutants are about 5% shorter than controls   (MGI Ref ID J:89242)
  • increased body weight   (MGI Ref ID J:5010)
    • by four weeks of age   (MGI Ref ID J:80996)
  • increased total body fat amount
    • increase in total fat content   (MGI Ref ID J:89242)
  • reproductive system phenotype
  • abnormal uterus morphology   (MGI Ref ID J:80996)
    • abnormal endometrium morphology
      • increased volume and density of lipid inclusion vacuoles   (MGI Ref ID J:80996)
      • basal membrane of epithelial cells displays a folded contour at locations where lipid accumulates   (MGI Ref ID J:80996)
      • tissue norepinephrin levels elevated by 4 weeks of age and remain elevated   (MGI Ref ID J:80996)
    • decreased uterus weight
      • decreased relative to controls by 4 weeks of age   (MGI Ref ID J:80996)
      • 1/3 normal tissue weight by 12 weeks   (MGI Ref ID J:80996)
  • vision/eye phenotype
  • abnormal intraocular pressure
    • modest but significant elevation of intraocular pressure   (MGI Ref ID J:82879)
  • behavior/neurological phenotype
  • abnormal conditioned taste aversion behavior
    • aversion response is more strongly generalized from saccharin to sucrose   (MGI Ref ID J:85127)
    • lower aversion threshold for sucrose than in controls   (MGI Ref ID J:85127)
    • recovery from conditioned taste aversion is more rapid than in controls   (MGI Ref ID J:85127)
  • polydipsia   (MGI Ref ID J:5010)
  • polyphagia   (MGI Ref ID J:5010)
  • renal/urinary system phenotype
  • abnormal kidney calyx morphology
    • calyceal dilation eventually develops   (MGI Ref ID J:5257)
  • abnormal kidney papilla morphology
    • eventually becomes flattened   (MGI Ref ID J:5257)
  • abnormal renal glomerulus morphology
    • large quantites if immunoglobulin and complement are found in the mesangium   (MGI Ref ID J:30970)
    • basement membrane becomes thickened with age   (MGI Ref ID J:5257)
  • increased urine protein level
    • in females when compared to female controls   (MGI Ref ID J:5257)
    • levels of protein in urine similar in males and females but levels in males lower than in male controls   (MGI Ref ID J:5257)
  • polyuria   (MGI Ref ID J:5010)
  • immune system phenotype
  • increased susceptibility to autoimmune diabetes
    • T cells from homozygous mice but not those from heterozygous mice suppressed the beta cell response to glucose + theophylline   (MGI Ref ID J:7005)
  • nervous system phenotype
  • abnormal hypothalamus physiology
    • hypothalamic uptake of norepinephrine is decreased in males   (MGI Ref ID J:1325)
  • adipose tissue phenotype
  • increased total body fat amount
    • increase in total fat content   (MGI Ref ID J:89242)
  • cardiovascular system phenotype
  • abnormal vascular wound healing
    • reduced neointimal area relative to controls 4 weeks after femoral artery injury   (MGI Ref ID J:135034)
    • vascular smooth muscle proliferation significantly reduced   (MGI Ref ID J:135034)
  • decreased systemic arterial blood pressure   (MGI Ref ID J:135034)

Leprdb/Leprdb

        C57BLKS/J
  • mortality/aging
  • increased sensitivity to induced morbidity/mortality
    • homozygotes subjected to 30, 45, and 60 min of left coronary artery ischemia-reperfusion exhibit survival rates of 71%, 53%, and 18%, respectively, at 24 h after reperfusion, much lower than in controls   (MGI Ref ID J:104790)
    • homozygotes subjected to 30 and 45 min of left coronary artery occlusion show survival rates of 58% and 44%, respectively, at 28 days after reperfusion, compared to 100% and 88% in controls   (MGI Ref ID J:104790)
  • behavior/neurological phenotype
  • polyphagia   (MGI Ref ID J:96047)
  • endocrine/exocrine gland phenotype
  • abnormal pancreatic islet morphology
    • islet mass and density are significantly increased compared to wild-type mice   (MGI Ref ID J:96047)
    • abnormal pancreatic beta cell morphology
      • individual beta cell size is increased   (MGI Ref ID J:96047)
  • growth/size/body phenotype
  • increased body weight
    • overweight by 4 weeks of age   (MGI Ref ID J:106597)
  • homeostasis/metabolism phenotype
  • abnormal glucose homeostasis
    • diabetic phenotype appears earlier in males than in females   (MGI Ref ID J:107138)
    • hyperglycemia   (MGI Ref ID J:104790)
    • increased circulating insulin level   (MGI Ref ID J:104790)
      • hyperinsulinemia by 8 weeks   (MGI Ref ID J:106597)
  • altered response to myocardial infarction
    • homozygotes subjected to 45 min of ischemia display an increase in diastolic dimensions, significant dilatation of left ventricular end-systolic dimensions, a 30% reduction in fractional shortening, and an increase in cardiac hypertrophy, 28 days postreperfusion, indicating decreased tolerance to myocardial infarction   (MGI Ref ID J:104790)
  • decreased body temperature   (MGI Ref ID J:96047)
  • hyperlipidemia   (MGI Ref ID J:96047)
  • increased circulating free fatty acid level   (MGI Ref ID J:106871)
  • increased glycosylated hemoglobin level
    • significant increase in the percentage of plasma glycosylated hemoglobin   (MGI Ref ID J:104790)
  • cardiovascular system phenotype
  • abnormal cardiovascular system physiology   (MGI Ref ID J:107138)
    • at low fatty acid supply, hearts consume 86% more oxygen (MVO2) for noncontractile purposes compared with control hearts and a further increase in fatty acid supply has no effect on the already elevated unloaded MVO2, indicating reduced cardiac efficiency in unloaded hearts   (MGI Ref ID J:106871)
    • abnormal blood circulation
      • reduced aortic flow   (MGI Ref ID J:107138)
      • cardiac ischemia
        • reduced recovery of mechanical function after 13 minutes of ischemia and reperfusion   (MGI Ref ID J:107138)
      • decreased cardiac output   (MGI Ref ID J:107138)
        • cardiac output is reduced in fatty acid perfused hearts   (MGI Ref ID J:106871)
    • altered response to myocardial infarction
      • homozygotes subjected to 45 min of ischemia display an increase in diastolic dimensions, significant dilatation of left ventricular end-systolic dimensions, a 30% reduction in fractional shortening, and an increase in cardiac hypertrophy, 28 days postreperfusion, indicating decreased tolerance to myocardial infarction   (MGI Ref ID J:104790)
    • decreased cardiac muscle contractility
      • hearts show a significant increase in the slope of the MVO2-PVA (pressure volume area) regression line after elevation of fatty acids, suggesting a reduction in contractile efficiency   (MGI Ref ID J:106871)
    • decreased heart rate   (MGI Ref ID J:107138)
      • intrinsic heart rates are reduced at all workloads   (MGI Ref ID J:106871)
    • decreased systemic arterial systolic blood pressure
      • decreased peak systolic pressure   (MGI Ref ID J:107138)
      • decreased peak systolic pressure X cardiac output   (MGI Ref ID J:107138)
      • decreased peak systolic pressure X heart rate   (MGI Ref ID J:107138)
    • increased left ventricle diastolic pressure
      • hearts show a significant increase in the slope of the MVO2-PVA (pressure volume area) regression line after elevation of fatty acids, suggesting a reduction in contractile efficiency   (MGI Ref ID J:106871)
    • increased vasoconstriction
      • hypercontractility of smooth muscle in aortic strips due to either phenylephrine or serotonin   (MGI Ref ID J:106597)
      • hypercontractility corrollated with the levels of obesity, hyperglycemia, and hyperinsulinemia   (MGI Ref ID J:106597)
      • maximal contractions increase with age rather than decrease as in controls   (MGI Ref ID J:106597)
  • abnormal myocardium layer morphology
    • myocardial triacylglycerol content 2X that of controls at 10-18 weeks of age   (MGI Ref ID J:107138)
  • hematopoietic system phenotype
  • increased glycosylated hemoglobin level
    • significant increase in the percentage of plasma glycosylated hemoglobin   (MGI Ref ID J:104790)
  • cellular phenotype
  • abnormal aerobic respiration
    • elevation of fatty acids in perfused hearts causes an increase in fatty acid oxidation combined with a reduction in glucose oxidation rates   (MGI Ref ID J:106871)
    • carbohydrate oxidation becomes reduced   (MGI Ref ID J:107138)
    • palmitate oxidation is elevated   (MGI Ref ID J:107138)
  • abnormal respiratory electron transport chain
    • state 3 respiration is elevated in cardiac mitochondria incubated with palmitoyl-carnitine but not with pyruvate   (MGI Ref ID J:106871)
  • muscle phenotype
  • decreased cardiac muscle contractility
    • hearts show a significant increase in the slope of the MVO2-PVA (pressure volume area) regression line after elevation of fatty acids, suggesting a reduction in contractile efficiency   (MGI Ref ID J:106871)
  • increased vasoconstriction
    • hypercontractility of smooth muscle in aortic strips due to either phenylephrine or serotonin   (MGI Ref ID J:106597)
    • hypercontractility corrollated with the levels of obesity, hyperglycemia, and hyperinsulinemia   (MGI Ref ID J:106597)
    • maximal contractions increase with age rather than decrease as in controls   (MGI Ref ID J:106597)

Leprdb/Leprdb

        BKS.Cg-Dock7m +/+ Leprdb/J
  • homeostasis/metabolism phenotype
  • abnormal circulating glucose level   (MGI Ref ID J:43162)
    • decreased circulating glucose level
      • brain derived neurotrophic factor (BDNF) causes a drop in blood glucose relative to controls 8 weeks after treatment   (MGI Ref ID J:43162)
      • affect of BDNF on blood glucose becomes progressively less as mice age   (MGI Ref ID J:43162)
      • neurotrophin 3 also causes a drop in blood glucose but the glucose levels return to normal by 24 hours after treatment   (MGI Ref ID J:43162)
      • glucose levels are reduced at all times tested when mice are placed on feeding restriction during the dark phase   (MGI Ref ID J:91813)
    • increased circulating glucose level
      • blood glucose shows a progressive increase from 5 through 33 weeks   (MGI Ref ID J:6323)
      • hyperglycemia   (MGI Ref ID J:185546)
        • fasting blood glucose level is significantly higher than control at 26 weeks of age   (MGI Ref ID J:135864)
  • abnormal circulating lipid level
    • plasma lipid levels differ between young and old mutants unlike on the C57BL/6J background where levels are similar at both ages; 14-month old mice have lower triglycerides, HDL cholesterol and combined VLDL + LDL cholesterol levels than 14-week old mice, but have significantly higher plasma triglyceride levels   (MGI Ref ID J:18161)
    • abnormal circulating cholesterol level   (MGI Ref ID J:18161)
      • increased circulating cholesterol level
        • fasting plasma total cholesterol concentration is increased 2 fold over controls   (MGI Ref ID J:18161)
        • increased circulating HDL cholesterol level   (MGI Ref ID J:18161)
        • increased circulating LDL cholesterol level   (MGI Ref ID J:18161)
        • increased circulating VLDL cholesterol level   (MGI Ref ID J:18161)
    • decreased circulating triglyceride level
      • triglyceride levels are reduced at all times tested when mice are placed on feeding restriction during the dark phase   (MGI Ref ID J:91813)
    • increased circulating triglyceride level
      • triglyceride levels are elevated 1.5- to 2-fold   (MGI Ref ID J:18161)
  • albuminuria
    • moderate albuminuria is observed at 26 weeks of age   (MGI Ref ID J:135864)
  • decreased circulating insulin level
    • BDNF causes a 50% reduction in plasma insulin relative to controls   (MGI Ref ID J:43162)
    • morning insulin levels lowered when feeding is restricted during the dark phase   (MGI Ref ID J:91813)
  • decreased prostaglandin level
    • in diabetic wounds, PGE2 level is consistently less than 50% of wild-type wounds at all times   (MGI Ref ID J:185546)
  • decreased urine albumin level
    • mutants treated with sRAGE do not show the increased albumin excretion seen in untreated mutants (0.11 ug albumin/ug creatinine vs 0.20 ug albumin/ ug creatinine); levels are not significantly different from control animals (0.08 ug albumin/ ug creatinine)   (MGI Ref ID J:82491)
  • delayed wound healing
    • wound healing is impaired, with an average wound closure time of 22 days, 7 days longer than in controls   (MGI Ref ID J:185546)
    • T26A, a prostaglandin transporter inhibitor, topically applied to wounds shortened wound closure to 16 days in mutants, similar to untreated controls; T26A increased re-epithelialization, neovascularization, and blood flow in wounds   (MGI Ref ID J:185546)
  • improved glucose tolerance
    • BDNF treatment causes a lower blood glucose level response in a glucose tolerance test   (MGI Ref ID J:43162)
  • increased glucagon secretion
    • increased secreation of glucagon by pancreatic cells in culture   (MGI Ref ID J:6264)
  • growth/size/body phenotype
  • increased body weight   (MGI Ref ID J:135864)
    • obese
      • become progressively obese starting at 5 weeks of age   (MGI Ref ID J:6323)
      • weight reaches 2.5X that of control mice by 3 months of age   (MGI Ref ID J:6323)
  • weight loss
    • body weight drops after 6 days on feeding restriction during the dark phase   (MGI Ref ID J:91813)
  • renal/urinary system phenotype
  • albuminuria
    • moderate albuminuria is observed at 26 weeks of age   (MGI Ref ID J:135864)
  • decreased urine albumin level
    • mutants treated with sRAGE do not show the increased albumin excretion seen in untreated mutants (0.11 ug albumin/ug creatinine vs 0.20 ug albumin/ ug creatinine); levels are not significantly different from control animals (0.08 ug albumin/ ug creatinine)   (MGI Ref ID J:82491)
  • expanded mesangial matrix
    • moderate mesangial expansion is observed in glomeruli at 26 weeks   (MGI Ref ID J:135864)
  • increased creatinine clearance
    • male mutants treated with sRAGE to achieve RAGE blockade display increased creatinine clearance (~5.1 ml/hour/100 x g body weight) compared to PBS-treated mutants (~3 ml/hour/100 x g body weight), approaching wild-type levels (6.7 ml/hour/100 x g body weight)   (MGI Ref ID J:82491)
  • nervous system phenotype
  • abnormal CNS synaptic transmission   (MGI Ref ID J:109401)
    • absent long term depression
      • CA1 hippocampal slices indicate no long term depression on recordings of excitatory post-synaptic potentials   (MGI Ref ID J:109401)
    • reduced long term potentiation
      • CA1 hippocampal slices indicate brief post tetanic potentiation but no long term potentiation on recordings of excitatory post-synaptic potentials   (MGI Ref ID J:109401)
  • abnormal nerve conduction
    • motor nerve conductance significantly lower than controls from 7 weeks of age onward   (MGI Ref ID J:6323)
    • velocity returns to and is maintained at prediabetic levels by 15 weeks of age whereas control mice show a continuous increase in velocity   (MGI Ref ID J:6323)
    • insulin treatment results in improved conductance but only for the duration of treatment and control levels of conductance are never restored   (MGI Ref ID J:6323)
    • no conductance improvement is seen in mice over 23 weeks in age due to insulin treatment   (MGI Ref ID J:6323)
  • abnormal nervous system morphology   (MGI Ref ID J:6323)
    • abnormal axon extension
      • axonal growth cone extension fails to occur for neurons treated in culture with 100ng/ml of leptin   (MGI Ref ID J:112680)
    • abnormal axon morphology
      • non significant shift toward smaller fiber diameter at 15 weeks of age   (MGI Ref ID J:6323)
      • significantly shifted to smaller diameter fibers by 25 weeks in ventral roots, dorsal roots, sural nerve   (MGI Ref ID J:6323)
      • smaller diameter nerve fibers in peroneal, phrenic and vagus nerves at 25 weeks but not significant   (MGI Ref ID J:6323)
      • small numbers of very large unmyelinated fibers (up to 1.6 micrometers)   (MGI Ref ID J:6323)
      • shift of unmyelinated fibers to smaller diameters   (MGI Ref ID J:6323)
      • abnormal myelin sheath morphology
        • number of myelin lamellae relative to nerve diameter is increased   (MGI Ref ID J:6323)
    • decreased motor neuron number
      • myelinated fibers reduced in numbers at 25 weeks in the sural nerve   (MGI Ref ID J:6323)
      • unmyelinated fibers reduced in numbers at 25 weeks in the vagus nerve   (MGI Ref ID J:6323)
      • myelinated fiber density increases in most nerves (not the peroneal and phrenic nerves)   (MGI Ref ID J:6323)
      • unmyelinated fiber density increase in the sural, peroneal, and vagus nerves   (MGI Ref ID J:6323)
  • behavior/neurological phenotype
  • abnormal circadian rhythm
    • daily locomotor pattern becomes attenuated in 6-8 week old mice but rhythmicity is retained   (MGI Ref ID J:91813)
    • daily locomotor activity rhythmicity severely diminished at 13-14 weeks, 75% fail to show significant rhythmicity   (MGI Ref ID J:91813)
    • daily locomotor rhythmicity restored by feeding restriction during dark phase   (MGI Ref ID J:91813)
  • abnormal food intake
    • food intake is about 60% of control level   (MGI Ref ID J:43162)
  • abnormal learning/memory/conditioning   (MGI Ref ID J:109401)
    • abnormal spatial learning
      • longer swimming distances than control mice in a Morris water maze test   (MGI Ref ID J:109401)
    • abnormal spatial reference memory
      • cross the original platform location less frequently than do controls in a Morris water maze test   (MGI Ref ID J:109401)
  • vision/eye phenotype
  • abnormal eye electrophysiology
    • prolonged latency of the b-wave in the retina   (MGI Ref ID J:103714)
    • delays in oscillatory potentials 1, 2, 3 although only the delay in "OP1" is significant   (MGI Ref ID J:103714)
  • endocrine/exocrine gland phenotype
  • increased glucagon secretion
    • increased secreation of glucagon by pancreatic cells in culture   (MGI Ref ID J:6264)
  • cardiovascular system phenotype
  • abnormal myocardial fiber morphology
    • presence of many lipid droplets   (MGI Ref ID J:6115)
    • dense bodies present in places normally occupied by mitochondria   (MGI Ref ID J:6115)
    • disrupted sarcomeres sometimes   (MGI Ref ID J:6115)
  • abnormal vascular development
    • dense bodies found in the smooth muscle of intramyocardial arteries   (MGI Ref ID J:6115)
  • muscle phenotype
  • abnormal myocardial fiber morphology
    • presence of many lipid droplets   (MGI Ref ID J:6115)
    • dense bodies present in places normally occupied by mitochondria   (MGI Ref ID J:6115)
    • disrupted sarcomeres sometimes   (MGI Ref ID J:6115)
  • cellular phenotype
  • abnormal axon extension
    • axonal growth cone extension fails to occur for neurons treated in culture with 100ng/ml of leptin   (MGI Ref ID J:112680)

Leprdb/Leprdb

        BKS.Cg-Dock7m +/+ Leprdb/OlaHsd
  • digestive/alimentary phenotype
  • abnormal digestive system physiology
    • transepithelial resistance in the epithelium is reduced, indictive of a disrupted mucosal barrier function   (MGI Ref ID J:124815)
  • abnormal intestinal epithelium morphology
    • reduced levels of occludin in intestinal sections   (MGI Ref ID J:124815)
    • zonula occludens 1 has a discontinuous distribution   (MGI Ref ID J:124815)
  • immune system phenotype
  • abnormal acute inflammation
    • higher levels of endotoxin are found in portal blood (entotoxemia)   (MGI Ref ID J:124815)
    • increased susceptibility to endotoxin shock
      • increased succeptibility of hepatic stellate cells to LPS   (MGI Ref ID J:124815)
  • abnormal chemokine secretion
    • increased release of monocyte chemo attractant protein by hepatic stellate cells   (MGI Ref ID J:124815)
  • increased interleukin-6 secretion
    • increased release by hepatic stellate cells   (MGI Ref ID J:124815)
  • liver inflammation   (MGI Ref ID J:124815)
  • liver/biliary system phenotype
  • liver inflammation   (MGI Ref ID J:124815)

Leprdb/Leprdb

        BKS.Cg-Dock7m +/+ Leprdb/Jcl
  • endocrine/exocrine gland phenotype
  • abnormal pancreas physiology
    • at 8 weeks, pancreatic islet cell proliferation is increased compared to in heterozygous mice   (MGI Ref ID J:156725)
    • however, pancreatic islet cell proliferation by 16 weeks is normal   (MGI Ref ID J:156725)
    • abnormal pancreatic islet cell apoptosis
      • pancreatic islet cell apoptosis is increased compared to in heterozygous mice   (MGI Ref ID J:156725)
  • increased pancreatic beta cell mass   (MGI Ref ID J:156725)
  • homeostasis/metabolism phenotype
  • hyperglycemia   (MGI Ref ID J:156725)
  • increased circulating insulin level   (MGI Ref ID J:156725)
  • adipose tissue phenotype
  • abnormal epididymal fat pad morphology
    • the epididymal fat pad exhibits macrophage infiltration unlike in wild-type mice   (MGI Ref ID J:110277)
  • cellular phenotype
  • abnormal pancreatic islet cell apoptosis
    • pancreatic islet cell apoptosis is increased compared to in heterozygous mice   (MGI Ref ID J:156725)

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

Dock7m/Dock7m

        DBA/J
  • pigmentation phenotype
  • diluted coat color
    • coat color is not as diluted as that of homozygous dilute (Myo5ad) or homozygous leaden (Mlphln) mice   (MGI Ref ID J:311)
    • individual hairs have more cortical pigment than found in homozygous dilute or homozygous leaden mice   (MGI Ref ID J:311)
  • variable body spotting
    • white tail tip with or without a white belly spot   (MGI Ref ID J:311)
  • integument phenotype
  • diluted coat color
    • coat color is not as diluted as that of homozygous dilute (Myo5ad) or homozygous leaden (Mlphln) mice   (MGI Ref ID J:311)
    • individual hairs have more cortical pigment than found in homozygous dilute or homozygous leaden mice   (MGI Ref ID J:311)
  • variable body spotting
    • white tail tip with or without a white belly spot   (MGI Ref ID J:311)

Dock7m/Dock7m

        B6.D(Cg)-Dock7m
  • adipose tissue phenotype
  • abnormal brown adipose tissue amount
    • appears to be completely absent in neonatal mice   (MGI Ref ID J:45425)
  • decreased white adipose tissue amount
    • mice have 21% less inguinal adipose mass   (MGI Ref ID J:48831)
  • growth/size/body phenotype
  • decreased body length
    • mutants are 8% shorter   (MGI Ref ID J:48831)
  • decreased body weight
    • mutants weigh 15% less   (MGI Ref ID J:48831)
  • hematopoietic system phenotype
  • decreased platelet ADP level
    • platelet ADP levels are low   (MGI Ref ID J:45425)
    • however, the platelet count, and platelet serotonin and ATP levels are normal   (MGI Ref ID J:45425)
  • homeostasis/metabolism phenotype
  • increased bleeding time   (MGI Ref ID J:45425)

Leprdb/Lepr+

        B6.Cg-Dock7m +/+ Leprdb/J
  • mortality/aging
  • extended life span
    • increased survival when totally deprived of food than wild-type controls   (MGI Ref ID J:6081)
    • survival when deprived of food is not as long as when in a C57BLKsS background   (MGI Ref ID J:6081)
  • growth/size/body phenotype
  • increased body weight
    • slight but significant increase in body weight compared to wild-type mice   (MGI Ref ID J:82334)

Leprdb/Leprdb

        FVB.BKS-Leprdb
  • growth/size/body phenotype
  • obese
    • mice of both sexes are obese   (MGI Ref ID J:78850)
  • homeostasis/metabolism phenotype
  • abnormal circulating glucose level
    • after a 2-day fast on refeeding with carbohydrate-free diet, female obese mice show a rise in glucose   (MGI Ref ID J:78850)
    • hyperglycemia
      • obese mice have a prolonged period of hyperglycemia compared to obese B6.BKS-Leprdb mice where glucose levels rarely exceed 250 mg/dl   (MGI Ref ID J:78850)
      • fasting mice are hyperglycemic at 3 months of age, while obese B6.BKS-Leprdb fasted mice are euglycemic   (MGI Ref ID J:78850)
      • levels increase from 5 to 7 months in obese females to ~500 ng/ml, significantly higher than the males (~40 ng/ml) or obese B6.BKS-Leprdb females (~50 ng/ml)   (MGI Ref ID J:78850)
  • impaired glucose tolerance
    • at 7 months of age obese males are severely glucose intolerant with glucose levels of >400 mg/dl 90 minutes after glucose load compared to obese B6.BKS-Leprdb mice clear glucose load by 90 min   (MGI Ref ID J:78850)
    • obese mice show a rapid increase of blood glucose above 400 mg/dl with diminished rate of glucose clearance   (MGI Ref ID J:78850)
  • increased circulating insulin level
    • at 3 months of age, females show a trend toward higher insulin levels compared to obese B6.BKS-Leprdb females; at 5-7 months insulin levels (~500 ng/ml) are ~10-fold higher than levels in obese female obese B6.BKS-Leprdb mice (~50 ng/ml)   (MGI Ref ID J:78850)
  • insulin resistance
    • at 7 months of age, 3U/kg of insulin does not alter circulating glucose levels, while in B6.BKS-Lepr mice, glucose decreases by 50% by 40 minutes; 12U/kg insulin does not cause a decrease in glucose in obese female mice on the FVB background   (MGI Ref ID J:78850)
    • at a dose of 3U/kg 6-week old mice show a diminished response to insulin   (MGI Ref ID J:78850)
    • circulating insulin levels in the fed state show that obese mice have exteme insulin resistance   (MGI Ref ID J:78850)
  • endocrine/exocrine gland phenotype
  • increased pancreatic beta cell number
    • obese mice show massive expansion of beta cells (744 insulin +ve cells/islet cross-section in obese vs 165 +ve cells in lean mice); there are 4.5-fold more cells per islet cross-section in obese mice   (MGI Ref ID J:78850)
  • pancreatic islet hyperplasia
    • some islets in obese mice have more than 1000 cells per cross section; such islets are absent in lean mice   (MGI Ref ID J:78850)
  • renal/urinary system phenotype
  • abnormal renal glomerulus morphology
    • at 7 months of age, obese mice show an increased mesangial matrix in most glomeruli compared to lean controls, resembling diabetic nephropathy; some small glomeruli have separated from the capsule with nearly obliterated microtubules   (MGI Ref ID J:78850)

Leprdb/Leprdb

        B6.Cg-Dock7m +/+ Leprdb/J
  • growth/size/body phenotype
  • decreased body length
    • snout to anus length is decreased by about 5% compared to wild-type mice   (MGI Ref ID J:82334)
  • obese
    • develop progressive obesity   (MGI Ref ID J:103063)
    • body weight is 2- to 3-fold more than in wild-type mice by 10 weeks of age   (MGI Ref ID J:82334)
    • body weight is 10% and 20% more in males and females, respectively, compared to Leprrtm1Mgmj homozygotes   (MGI Ref ID J:82334)
    • increase in body weight becomes apparent at 4-6 weeks of age   (MGI Ref ID J:18161)
  • behavior/neurological phenotype
  • polyphagia   (MGI Ref ID J:82334)
  • reduced male mating frequency   (MGI Ref ID J:6157)
  • cardiovascular system phenotype
  • abnormal myocardial fiber morphology
    • exhibit myocyte hypertrophy   (MGI Ref ID J:103063)
  • heart left ventricle hypertrophy
    • increase in left ventricle wall thickness and mass is seen by 6 months of age but not at 2 months of age   (MGI Ref ID J:103063)
    • induced weight loss via leptin infusion, but not via caloric restriction, partially resolves the hypertrophy   (MGI Ref ID J:103063)
  • muscle phenotype
  • abnormal myocardial fiber morphology
    • exhibit myocyte hypertrophy   (MGI Ref ID J:103063)
  • homeostasis/metabolism phenotype
  • abnormal chemokine level
    • elevated levels of eotaxin, keratinocyte cytokine, and monocyte chemotactic protein-1 (also elevated in serum) in bronchoalveolar lavage fluid   (MGI Ref ID J:115772)
  • abnormal circulating lipid level
    • HDL cholesterol and glucose levels increase concurrently   (MGI Ref ID J:18161)
    • plasma lipid levels are similar at 3.5 and 14 months of age on the C57BL/6J background unlike on a C57BL/KsJ background   (MGI Ref ID J:18161)
    • abnormal circulating cholesterol level   (MGI Ref ID J:18161)
      • increased circulating cholesterol level
        • fasting plasma total cholesterol concentration is increased 2 fold over controls   (MGI Ref ID J:18161)
        • increased circulating HDL cholesterol level   (MGI Ref ID J:18161)
        • increased circulating LDL cholesterol level   (MGI Ref ID J:18161)
        • increased circulating VLDL cholesterol level   (MGI Ref ID J:18161)
    • increased circulating triglyceride level   (MGI Ref ID J:82334)
      • triglyceride levels are elevated 1.5- to 2-fold   (MGI Ref ID J:18161)
  • abnormal glucose homeostasis   (MGI Ref ID J:82334)
    • increased circulating glucose level   (MGI Ref ID J:82334)
      • hyperglycemia   (MGI Ref ID J:18161)
    • increased circulating insulin level   (MGI Ref ID J:82334)
  • abnormal hormone level
    • female mice exhibit an increase in hypothalamic gonadotrophin releasing hormone compared to in wild-type mice   (MGI Ref ID J:6157)
    • decreased adiponectin level
      • decreased in serum   (MGI Ref ID J:115772)
    • increased circulating insulin level   (MGI Ref ID J:82334)
    • increased circulating leptin level   (MGI Ref ID J:115772)
  • abnormal interleukin level
    • elevated levels of IL-6 in bronchoalveolar lavage fluid   (MGI Ref ID J:115772)
    • increased circulating interleukin-6 level
      • elevated levels of IL-6 in serum   (MGI Ref ID J:115772)
  • reproductive system phenotype
  • abnormal female reproductive system morphology
    • atrophy of the reproductive organs   (MGI Ref ID J:82334)
    • constricted vagina orifice   (MGI Ref ID J:6157)
    • small uterus   (MGI Ref ID J:6157)
  • absent estrous cycle
    • mice exhibit diestrous vaginal acyclicity or occasional metestrous acyclicity   (MGI Ref ID J:6157)
  • absent estrus
    • females never show signs of vaginal oestrous   (MGI Ref ID J:82334)
  • anovulation   (MGI Ref ID J:82334)
  • female infertility   (MGI Ref ID J:6157)
    • all females fail to reproduce   (MGI Ref ID J:82334)
  • respiratory system phenotype
  • abnormal functional residual capacity
    • reduced   (MGI Ref ID J:115772)
    • pressure volume curves shifted to the right   (MGI Ref ID J:115772)
  • abnormal respiratory mechanics
    • end-expiratory pause increases considerably less than in controls after ozone exposure   (MGI Ref ID J:115772)
    • abnormal lung compliance
      • total lung resistance increases much more in response to ozone than in control mice   (MGI Ref ID J:115772)
      • responsiveness to methacholine and serotonin is much greater than controls   (MGI Ref ID J:115772)
    • decreased pulmonary ventilation
      • ventilation volumes decline with ozone exposure but to a lesser degree than for controls   (MGI Ref ID J:115772)
  • lung inflammation
    • elevated levels of eotaxin, Il6, keratinocyte cytokine, monocyte chemotactic protein-1, and neutrophiles in bronchoalveolar lavage as a result of ozone exposure   (MGI Ref ID J:115772)
    • ozone induces significantly elevated levels of TNFR1   (MGI Ref ID J:115772)
    • ozone induces a nonsignificant elevation of TNFR2 levels   (MGI Ref ID J:115772)
    • elevated pulmonary levels of Il1beta mRNA 24 hours after ozone exposure   (MGI Ref ID J:115772)
    • elevated pulmonary levels of TNF mRNA 24 hours after ozone exposure but to a lesser extent than in controls   (MGI Ref ID J:115772)
  • immune system phenotype
  • abnormal chemokine level
    • elevated levels of eotaxin, keratinocyte cytokine, and monocyte chemotactic protein-1 (also elevated in serum) in bronchoalveolar lavage fluid   (MGI Ref ID J:115772)
  • abnormal interleukin level
    • elevated levels of IL-6 in bronchoalveolar lavage fluid   (MGI Ref ID J:115772)
    • increased circulating interleukin-6 level
      • elevated levels of IL-6 in serum   (MGI Ref ID J:115772)
  • abnormal leukocyte morphology   (MGI Ref ID J:115772)
    • decreased leukocyte cell number
      • decrease blood leukocyte numbers   (MGI Ref ID J:115772)
    • increased neutrophil cell number
      • increased numbers in bronchoalveolar lavage   (MGI Ref ID J:115772)
  • lung inflammation
    • elevated levels of eotaxin, Il6, keratinocyte cytokine, monocyte chemotactic protein-1, and neutrophiles in bronchoalveolar lavage as a result of ozone exposure   (MGI Ref ID J:115772)
    • ozone induces significantly elevated levels of TNFR1   (MGI Ref ID J:115772)
    • ozone induces a nonsignificant elevation of TNFR2 levels   (MGI Ref ID J:115772)
    • elevated pulmonary levels of Il1beta mRNA 24 hours after ozone exposure   (MGI Ref ID J:115772)
    • elevated pulmonary levels of TNF mRNA 24 hours after ozone exposure but to a lesser extent than in controls   (MGI Ref ID J:115772)
  • tumorigenesis
  • increased metastatic potential
    • increased metastasis to the lung of both melanoma cell lines and lung cancer cell lines initially injected in the tail vein   (MGI Ref ID J:117826)
  • hematopoietic system phenotype
  • abnormal leukocyte morphology   (MGI Ref ID J:115772)
    • decreased leukocyte cell number
      • decrease blood leukocyte numbers   (MGI Ref ID J:115772)
    • increased neutrophil cell number
      • increased numbers in bronchoalveolar lavage   (MGI Ref ID J:115772)
  • nervous system phenotype
  • abnormal hypothalamus physiology   (MGI Ref ID J:6157)

Leprdb/Leprdb

        involves: 129S2/SvPas * C57BL/6 * C57BLKS/J
  • renal/urinary system phenotype
  • abnormal kidney morphology
    • total kidney collagen is increased in females by 96%   (MGI Ref ID J:127478)
    • abnormal renal glomerulus morphology
      • glomerular extracellular matrix (ECM) area in females is increased by 31% compared to wild-type female controls and female single Serpine1-deficient animals; however, when expressed as fractional glomerular ECM area, little difference is observed between any genotype   (MGI Ref ID J:127478)

Leprdb/Leprdb

        involves: C57BL/6 * C57BLKS/J
  • reproductive system phenotype
  • abnormal female reproductive system morphology   (MGI Ref ID J:164339)
  • absent estrus   (MGI Ref ID J:164339)
  • female infertility   (MGI Ref ID J:142218)
  • homeostasis/metabolism phenotype
  • abnormal oxygen consumption
    • oxygen consumption normalized to lean mass is increased compared to wild-type controls but oxygen consumption normalized to metabolic size is decreased compared to wild-type controls   (MGI Ref ID J:142218)
  • impaired adaptive thermogenesis
    • thermoregulation in response to cold exposure is severely impaired compared to wild-type controls   (MGI Ref ID J:142218)
  • impaired glucose tolerance   (MGI Ref ID J:142218)
  • increased circulating glucose level   (MGI Ref ID J:164339)
    • hyperglycemia   (MGI Ref ID J:142218)
  • increased circulating insulin level   (MGI Ref ID J:164339)
  • increased circulating leptin level   (MGI Ref ID J:142218)
  • insulin resistance   (MGI Ref ID J:142218)
  • growth/size/body phenotype
  • decreased body length   (MGI Ref ID J:142218)
  • decreased lean body mass   (MGI Ref ID J:164339)
  • increased body weight   (MGI Ref ID J:164339)
    • obese
      • early onset obesity starting from 4 weeks of age   (MGI Ref ID J:142218)
  • increased percent body fat   (MGI Ref ID J:142218)
  • adipose tissue phenotype
  • increased percent body fat   (MGI Ref ID J:142218)
  • behavior/neurological phenotype
  • abnormal eating behavior   (MGI Ref ID J:164339)
  • hypoactivity
    • decreased activity in both the light and dark cycle   (MGI Ref ID J:142218)
  • limbs/digits/tail phenotype
  • short femur   (MGI Ref ID J:164339)
  • skeleton phenotype
  • short femur   (MGI Ref ID J:164339)

Leprdb/Leprdb

        B6.BKS(D)-Leprdb/J
  • homeostasis/metabolism phenotype
  • abnormal response/metabolism to endogenous compounds
    • mice treated with leptin fail to exhibit a decrease in food intake unlike similarly treated wild-type mice   (MGI Ref ID J:166105)
  • decreased body temperature   (MGI Ref ID J:166105)
  • decreased carbon dioxide production   (MGI Ref ID J:166105)
  • decreased oxygen consumption   (MGI Ref ID J:166105)
  • impaired glucose tolerance   (MGI Ref ID J:166105)
  • insulin resistance   (MGI Ref ID J:166105)
  • behavior/neurological phenotype
  • abnormal behavior
    • faster in food finding trials relative to controls   (MGI Ref ID J:112820)
    • hypoactivity
      • during the dark phase   (MGI Ref ID J:166105)
  • renal/urinary system phenotype
  • glomerulosclerosis
    • homozygotes develop significant glomerulosclerosis by 18 weeks of age   (MGI Ref ID J:160943)
View Research Applications

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

Diabetes and Obesity Research
Hyperglycemia
Type 2 Diabetes (NIDDM)

Internal/Organ Research
Wound Healing
      delayed/impaired

Dock7m related

Dermatology Research
Color and White Spotting Defects

Leprdb related

Diabetes and Obesity Research
Hyperinsulinemia
Impaired Wound Healing
Insulin Resistance
Obesity With Diabetes

Endocrine Deficiency Research
Adipose Defects
Hypothalamus/Pituitary Defects
Pancreas Defects

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency Associated with Other Defects

Internal/Organ Research
Adipose Defects

Metabolism Research

Reproductive Biology Research
Fertility Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Dock7m
Allele Name misty
Allele Type Spontaneous
Common Name(s) m;
Strain of OriginDBA/J
Gene Symbol and Name Dock7, dedicator of cytokinesis 7
Chromosome 4
Gene Common Name(s) 3110056M06Rik; EIEE23; Gm430; LOC242555; RIKEN cDNA 3110056M06 gene; ZIR2; gene model 430, (NCBI); m; mKIAA1771; misty;
Molecular Note Crosses between mice homozygous for misty and for moonlight, which mapped to overlapping critical regions on Chr 4, demonstrated failure of the two mutations to complement one another. Once moonlight had been identified as a mutation of Dock7 (Dock7mnlt), sequence analysis of this gene from misty mice revealed a retrotransposon LTR insertion following nucleotide 2045 (numbering from the A of the transcription initiation codon) that interrupts exon 18 and shifts the reading frame after codon 682 so that ten incorrect amino acids are incorporated into the protein before its premature termination. [MGI Ref ID J:146458]
 
Allele Symbol Leprdb
Allele Name diabetes
Allele Type Spontaneous
Common Name(s) Lepdb; Lepr-; Leprdb-1J; db; db/db; leprdb;
Strain of OriginC57BLKS/J
Gene Symbol and Name Lepr, leptin receptor
Chromosome 4
Gene Common Name(s) CD295; Fa; LEP-R; LEPRD; LEPROT; Leprb; Modb1; OB-R; OB-RGRP; OBR; db; diabetes; leptin receptor gene-related protein; obese-like; obl;
Molecular Note A G-to-T transversion in this allele created a donor splice site that causes abnormal splicing and a 106 nt insertion in the transcript, leading to premature termination of the long cellular domain of the Ob-Rb splice form and loss of its signal transducing function. [MGI Ref ID J:31324] [MGI Ref ID J:31327] [MGI Ref ID J:31488]

Genotyping

Genotyping Information

Genotyping Protocols

Dock7m qPCR, QPCR
Lepr db, End Point Analysis
Leprdb, Restriction Enzyme Digest


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Chen H; Charlat O; Tartaglia LA; Woolf EA; Weng X; Ellis SJ; Lakey ND; Culpepper J; Moore KJ; Breitbart RE; Duyk GM; Tepper RI; Morgenstern JP. 1996. Evidence that the diabetes gene encodes the leptin receptor: identification of a mutation in the leptin receptor gene in db/db mice. Cell 84(3):491-5. [PubMed: 8608603]  [MGI Ref ID J:31324]

Chua SC Jr; Chung WK; Wu-Peng XS; Zhang Y; Liu SM; Tartaglia L; Leibel RL. 1996. Phenotypes of mouse diabetes and rat fatty due to mutations in the OB (leptin) receptor [see comments] Science 271(5251):994-6. [PubMed: 8584938]  [MGI Ref ID J:31419]

Dardenne M; Savino W; Bach JF. 1984. Autoimmune mice develop antibodies to thymic hormone: production of anti-thymulin monoclonal autoantibodies from diabetic (db/db) and B/W mice. J Immunol 133(2):740-3. [PubMed: 6539799]  [MGI Ref ID J:109953]

Fantuzzi G; Faggioni R. 2000. Leptin in the regulation of immunity, inflammation, and hematopoiesis. J Leukoc Biol 68(4):437-46. [PubMed: 11037963]  [MGI Ref ID J:109886]

Gueorguiev M; Goth ML; Korbonits M. 2001. Leptin and puberty: a review. Pituitary 4(1-2):79-86. [PubMed: 11824512]  [MGI Ref ID J:109856]

Hummel KP; Dickie MM; Coleman DL. 1966. Diabetes, a new mutation in the mouse. Science 153(740):1127-8. [PubMed: 5918576]  [MGI Ref ID J:5010]

Kampfer H; Paulukat J; Muhl H; Wetzler C; Pfeilschifter J; Frank S. 2000. Lack of interferon-gamma production despite the presence of interleukin-18 during cutaneous wound healing. Mol Med 6(12):1016-27. [PubMed: 11474118]  [MGI Ref ID J:109870]

Lee GH; Proenca R; Montez JM; Carroll KM; Darvishzadeh JG; Lee JI; Friedman JM. 1996. Abnormal splicing of the leptin receptor in diabetic mice. Nature 379(6566):632-5. [PubMed: 8628397]  [MGI Ref ID J:31327]

Leiter EH; Chapman HD. 1994. Obesity-induced diabetes (diabesity) in C57BL/KsJ mice produces aberrant trans-regulation of sex steroid sulfotransferase genes. J Clin Invest 93(5):2007-13. [PubMed: 8182132]  [MGI Ref ID J:17991]

Mandel MA; Mahmoud AA. 1978. Impairment of cell-mediated immunity in mutation diabetic mice (db/db). J Immunol 120(4):1375-7. [PubMed: 347001]  [MGI Ref ID J:109964]

Serreze DV; Leiter EH; Kuff EL; Jardieu P; Ishizaka K. 1988. Molecular mimicry between insulin and retroviral antigen p73. Development of cross-reactive autoantibodies in sera of NOD and C57BL/KsJ db/db mice. Diabetes 37(3):351-8. [PubMed: 3286334]  [MGI Ref ID J:27625]

Yoon JW; Leiter EH; Coleman DL; Kim MK; Pak CY; McArthur RG; Roncari DA. 1988. Genetic control of organ-reactive autoantibody production in mice by obesity (ob) diabetes (db) genes. Diabetes 37(9):1287-93. [PubMed: 3044893]  [MGI Ref ID J:109940]

Additional References

Bahary N; Leibel RL; Joseph L; Friedman JM. 1990. Molecular mapping of the mouse db mutation. Proc Natl Acad Sci U S A 87(21):8642-6. [PubMed: 1978328]  [MGI Ref ID J:10819]

Barinaga M. 1996. Researchers nail down leptin receptor [news; comment] Science 271(5251):913. [PubMed: 8584929]  [MGI Ref ID J:31488]

Bouchard G; Johnson D; Carver T; Paigen B; Carey MC. 2002. Cholesterol gallstone formation in overweight mice establishes that obesity per se is not linked directly to cholelithiasis risk. J Lipid Res 43(7):1105-13. [PubMed: 12091495]  [MGI Ref ID J:88773]

Cohen MP; Sharma K; Jin Y; Hud E; Wu VY; Tomaszewski J; Ziyadeh FN. 1995. Prevention of diabetic nephropathy in db/db mice with glycated albumin antagonists. A novel treatment strategy. J Clin Invest 95(5):2338-45. [PubMed: 7738197]  [MGI Ref ID J:24919]

Coleman DL. 1978. Obese and diabetes: two mutant genes causing diabetes-obesity syndromes in mice. Diabetologia 14(3):141-8. [PubMed: 350680]  [MGI Ref ID J:5986]

Coleman DL. 1979. Obesity genes: beneficial effects in heterozygous mice. Science 203(4381):663-5. [PubMed: 760211]  [MGI Ref ID J:6081]

Coleman DL; Hummel KP. 1973. The influence of genetic background on the expression of the obese (Ob) gene in the mouse. Diabetologia 9(4):287-93. [PubMed: 4588246]  [MGI Ref ID J:5400]

Debray-Sachs M; Sai P; Boitard C; Assan R; Hamburger J. 1983. Anti-pancreatic immunity in genetically diabetic mice. Clin Exp Immunol 51(1):1-7. [PubMed: 6339122]  [MGI Ref ID J:7005]

Di Marzo V; Goparaju SK; Wang L; Liu J; Batkai S; Jarai Z; Fezza F; Miura GI; Palmiter RD; Sugiura T; Kunos G. 2001. Leptin-regulated endocannabinoids are involved in maintaining food intake. Nature 410(6830):822-5. [PubMed: 11298451]  [MGI Ref ID J:68834]

Fiedorek FT Jr; Kay ES. 1994. Mapping of PCR-based markers for mouse chromosome 4 on a backcross penetrant for the misty (m) mutation. Mamm Genome 5(8):479-85. [PubMed: 7949731]  [MGI Ref ID J:20039]

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Yamauchi T; Nio Y; Maki T; Kobayashi M; Takazawa T; Iwabu M; Okada-Iwabu M; Kawamoto S; Kubota N; Kubota T; Ito Y; Kamon J; Tsuchida A; Kumagai K; Kozono H; Hada Y; Ogata H; Tokuyama K; Tsunoda M; Ide T; Murakami K; Awazawa M; Takamoto I; Froguel P; HaraK; Tobe K; Nagai R; Ueki K; Kadowaki T. 2007. Targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and metabolic actions Nat Med 13(3):332-339. [PubMed: 17268472]  [MGI Ref ID J:117919]

Yan L; Guo S; Brault M; Harmon J; Robertson RP; Hamid R; Stein R; Yang E. 2012. The B55alpha-containing PP2A holoenzyme dephosphorylates FOXO1 in islet beta-cells under oxidative stress. Biochem J 444(2):239-47. [PubMed: 22417654]  [MGI Ref ID J:185464]

Yan QW; Yang Q; Mody N; Graham TE; Hsu CH; Xu Z; Houstis NE; Kahn BB; Rosen ED. 2007. The adipokine lipocalin 2 is regulated by obesity and promotes insulin resistance. Diabetes 56(10):2533-40. [PubMed: 17639021]  [MGI Ref ID J:126560]

Yang J; Park Y; Zhang H; Gao X; Wilson E; Zimmer W; Abbott L; Zhang C. 2009. Role of MCP-1 in tumor necrosis factor-alpha-induced endothelial dysfunction in type 2 diabetic mice. Am J Physiol Heart Circ Physiol 297(4):H1208-16. [PubMed: 19666844]  [MGI Ref ID J:154217]

Yang J; Park Y; Zhang H; Xu X; Laine GA; Dellsperger KC; Zhang C. 2009. Feed-forward signaling of TNF-alpha and NF-kappaB via IKK-beta pathway contributes to insulin resistance and coronary arteriolar dysfunction in type 2 diabetic mice. Am J Physiol Heart Circ Physiol 296(6):H1850-8. [PubMed: 19363130]  [MGI Ref ID J:150876]

Yang S; Chen C; Wang H; Rao X; Wang F; Duan Q; Chen F; Long G; Gong W; Zou MH; Wang DW. 2012. Protective effects of Acyl-coA thioesterase 1 on diabetic heart via PPARalpha/PGC1alpha signaling. PLoS One 7(11):e50376. [PubMed: 23226270]  [MGI Ref ID J:195446]

Yang Y; Gurung B; Wu T; Wang H; Stoffers DA; Hua X. 2010. Reversal of preexisting hyperglycemia in diabetic mice by acute deletion of the Men1 gene. Proc Natl Acad Sci U S A 107(47):20358-63. [PubMed: 21059956]  [MGI Ref ID J:166586]

Yano H; Kinoshita M; Fujino K; Nakashima M; Yamamoto Y; Miyazaki H; Hamada K; Ono S; Iwaya K; Saitoh D; Seki S; Tanaka Y. 2012. Insulin treatment directly restores neutrophil phagocytosis and bactericidal activity in diabetic mice and thereby improves surgical site Staphylococcus aureus infection. Infect Immun 80(12):4409-16. [PubMed: 23027538]  [MGI Ref ID J:190600]

Ye Y; Qian J; Castillo AC; Ling S; Ye H; Perez-Polo JR; Bajaj M; Birnbaum Y. 2013. Phosphodiesterase-3 inhibition augments the myocardial infarct size-limiting effects of exenatide in mice with type 2 diabetes. Am J Physiol Heart Circ Physiol 304(1):H131-41. [PubMed: 23103492]  [MGI Ref ID J:192851]

Yi P; Park JS; Melton DA. 2013. Betatrophin: a hormone that controls pancreatic beta cell proliferation. Cell 153(4):747-58. [PubMed: 23623304]  [MGI Ref ID J:197679]

Yin L; Ma H; Ge X; Edwards PA; Zhang Y. 2011. Hepatic hepatocyte nuclear factor 4alpha is essential for maintaining triglyceride and cholesterol homeostasis. Arterioscler Thromb Vasc Biol 31(2):328-36. [PubMed: 21071704]  [MGI Ref ID J:184185]

Yin W; Carballo-Jane E; McLaren DG; Mendoza VH; Gagen K; Geoghagen NS; McNamara LA; Gorski JN; Eiermann GJ; Petrov A; Wolff M; Tong X; Wilsie LC; Akiyama TE; Chen J; Thankappan A; Xue J; Ping X; Andrews G; Wickham LA; Gai CL; Trinh T; Kulick AA; DonnellyMJ; Voronin GO; Rosa R; Cumiskey AM; Bekkari K; Mitnaul LJ; Puig O; Chen F; Raubertas R; Wong PH; Hansen BC; Koblan KS; Roddy TP; Hubbard BK; Strack AM. 2012. Plasma lipid profiling across species for the identification of optimal animal models of human dyslipidemia. J Lipid Res 53(1):51-65. [PubMed: 22021650]  [MGI Ref ID J:179410]

Yu F; Li BY; Li XL; Cai Q; Zhang Z; Cheng M; Yin M; Wang JF; Zhang JH; Lu WD; Zhou RH; Gao HQ. 2012. Proteomic analysis of aorta and protective effects of grape seed procyanidin B2 in db/db mice reveal a critical role of milk fat globule epidermal growth factor-8 in diabetic arterial damage. PLoS One 7(12):e52541. [PubMed: 23285083]  [MGI Ref ID J:195760]

Yu X; Shen N; Zhang ML; Pan FY; Wang C; Jia WP; Liu C; Gao Q; Gao X; Xue B; Li CJ. 2011. Egr-1 decreases adipocyte insulin sensitivity by tilting PI3K/Akt and MAPK signal balance in mice. EMBO J 30(18):3754-65. [PubMed: 21829168]  [MGI Ref ID J:179942]

Yu Y; Liu Y; Shi FD; Zou H; Matarese G; La Cava A. 2013. Cutting Edge: Leptin-Induced RORgammat Expression in CD4+ T Cells Promotes Th17 Responses in Systemic Lupus Erythematosus. J Immunol 190(7):3054-8. [PubMed: 23447682]  [MGI Ref ID J:194839]

Yuan H; Reddy MA; Sun G; Lanting L; Wang M; Kato M; Natarajan R. 2013. Involvement of p300/CBP and epigenetic histone acetylation in TGF-beta1-mediated gene transcription in mesangial cells. Am J Physiol Renal Physiol 304(5):F601-13. [PubMed: 23235480]  [MGI Ref ID J:193183]

Yue P; Arai T; Terashima M; Sheikh AY; Cao F; Charo D; Hoyt G; Robbins RC; Ashley EA; Wu J; Yang PC; Tsao PS. 2007. Magnetic resonance imaging of progressive cardiomyopathic changes in the db/db mouse. Am J Physiol Heart Circ Physiol 292(5):H2106-18. [PubMed: 17122193]  [MGI Ref ID J:126005]

Yue P; Jin H; Aillaud M; Deng AC; Azuma J; Asagami T; Kundu RK; Reaven GM; Quertermous T; Tsao PS. 2010. Apelin is necessary for the maintenance of insulin sensitivity. Am J Physiol Endocrinol Metab 298(1):E59-67. [PubMed: 19861585]  [MGI Ref ID J:170135]

Yusta B; Baggio LL; Estall JL; Koehler JA; Holland DP; Li H; Pipeleers D; Ling Z; Drucker DJ. 2006. GLP-1 receptor activation improves beta cell function and survival following induction of endoplasmic reticulum stress. Cell Metab 4(5):391-406. [PubMed: 17084712]  [MGI Ref ID J:129760]

Zeng H; He X; Hou X; Li L; Chen JX. 2014. Apelin gene therapy increases myocardial vascular density and ameliorates diabetic cardiomyopathy via upregulation of sirtuin 3. Am J Physiol Heart Circ Physiol 306(4):H585-97. [PubMed: 24363305]  [MGI Ref ID J:208696]

Zenker J; Poirot O; de Preux Charles AS; Arnaud E; Medard JJ; Lacroix C; Kuntzer T; Chrast R. 2012. Altered distribution of juxtaparanodal kv1.2 subunits mediates peripheral nerve hyperexcitability in type 2 diabetes mellitus. J Neurosci 32(22):7493-8. [PubMed: 22649228]  [MGI Ref ID J:184972]

Zhang F; Dey D; Branstrom R; Forsberg L; Lu M; Zhang Q; Sjoholm A. 2009. BLX-1002, a novel thiazolidinedione with no PPAR affinity, stimulates AMP-activated protein kinase activity, raises cytosolic Ca2+, and enhances glucose-stimulated insulin secretion in a PI3K-dependent manner. Am J Physiol Cell Physiol 296(2):C346-54. [PubMed: 19052259]  [MGI Ref ID J:146323]

Zhang H; Park Y; Zhang C. 2010. Coronary and aortic endothelial function affected by feedback between adiponectin and tumor necrosis factor alpha in type 2 diabetic mice. Arterioscler Thromb Vasc Biol 30(11):2156-63. [PubMed: 20814014]  [MGI Ref ID J:182099]

Zhang H; Zhang J; Ungvari Z; Zhang C. 2009. Resveratrol improves endothelial function: role of TNF{alpha} and vascular oxidative stress. Arterioscler Thromb Vasc Biol 29(8):1164-71. [PubMed: 19478208]  [MGI Ref ID J:167814]

Zhang HM; Dang H; Kamat A; Yeh CK; Zhang BX. 2012. Geldanamycin derivative ameliorates high fat diet-induced renal failure in diabetes. PLoS One 7(3):e32746. [PubMed: 22412919]  [MGI Ref ID J:186932]

Zhang K; Li L; Qi Y; Zhu X; Gan B; DePinho RA; Averitt T; Guo S. 2012. Hepatic suppression of Foxo1 and Foxo3 causes hypoglycemia and hyperlipidemia in mice. Endocrinology 153(2):631-46. [PubMed: 22147007]  [MGI Ref ID J:181743]

Zhang LL; Yan Liu D; Ma LQ; Luo ZD; Cao TB; Zhong J; Yan ZC; Wang LJ; Zhao ZG; Zhu SJ; Schrader M; Thilo F; Zhu ZM; Tepel M. 2007. Activation of transient receptor potential vanilloid type-1 channel prevents adipogenesis and obesity. Circ Res 100(7):1063-70. [PubMed: 17347480]  [MGI Ref ID J:133914]

Zhang LN; Zhou HY; Fu YY; Li YY; Wu F; Gu M; Wu LY; Xia CM; Dong TC; Li JY; Shen JK; Li J. 2013. Novel small-molecule PGC-1alpha transcriptional regulator with beneficial effects on diabetic db/db mice. Diabetes 62(4):1297-307. [PubMed: 23250358]  [MGI Ref ID J:208587]

Zhang M; Zhu Y; Mu K; Li L; Lu J; Zhao J; Huang X; Wang C; Jia W. 2013. Loss of beta-arrestin2 mediates pancreatic-islet dysfunction in mice. Biochem Biophys Res Commun 435(3):345-9. [PubMed: 23660189]  [MGI Ref ID J:202642]

Zhang Q; Zhu Y; Zhou W; Gao L; Yuan L; Han X. 2013. Serotonin receptor 2C and insulin secretion. PLoS One 8(1):e54250. [PubMed: 23349838]  [MGI Ref ID J:195843]

Zhang X; Yeung DC; Karpisek M; Stejskal D; Zhou ZG; Liu F; Wong RL; Chow WS; Tso AW; Lam KS; Xu A. 2008. Serum FGF21 levels are increased in obesity and are independently associated with the metabolic syndrome in humans. Diabetes 57(5):1246-53. [PubMed: 18252893]  [MGI Ref ID J:135319]

Zhang X; Zhang G; Zhang H; Karin M; Bai H; Cai D. 2008. Hypothalamic IKKbeta/NF-kappaB and ER stress link overnutrition to energy imbalance and obesity. Cell 135(1):61-73. [PubMed: 18854155]  [MGI Ref ID J:149873]

Zhang Y; Gan Z; Huang P; Zhou L; Mao T; Shao M; Jiang X; Chen Y; Ying H; Cao M; Li J; Li J; Zhang WJ; Yang L; Liu Y. 2012. A role for protein inhibitor of activated STAT1 (PIAS1) in lipogenic regulation through SUMOylation-independent suppression of liver X receptors. J Biol Chem 287(45):37973-85. [PubMed: 22969086]  [MGI Ref ID J:192963]

Zhang Y; Lee FY; Barrera G; Lee H; Vales C; Gonzalez FJ; Willson TM; Edwards PA. 2006. Activation of the nuclear receptor FXR improves hyperglycemia and hyperlipidemia in diabetic mice. Proc Natl Acad Sci U S A 103(4):1006-11. [PubMed: 16410358]  [MGI Ref ID J:105654]

Zhang Y; Yuen DA; Advani A; Thai K; Advani SL; Kepecs D; Kabir MG; Connelly KA; Gilbert RE. 2012. Early-outgrowth bone marrow cells attenuate renal injury and dysfunction via an antioxidant effect in a mouse model of type 2 diabetes. Diabetes 61(8):2114-25. [PubMed: 22596053]  [MGI Ref ID J:208456]

Zhang Z; Li BY; Li XL; Cheng M; Yu F; Lu WD; Cai Q; Wang JF; Zhou RH; Gao HQ; Shen L. 2013. Proteomic analysis of kidney and protective effects of grape seed procyanidin B2 in db/db mice indicate MFG-E8 as a key molecule in the development of diabetic nephropathy. Biochim Biophys Acta 1832(6):805-16. [PubMed: 23474305]  [MGI Ref ID J:202424]

Zhang Z; Luo X; Ding S; Chen J; Chen T; Chen X; Zha H; Yao L; He X; Peng H. 2012. MicroRNA-451 regulates p38 MAPK signaling by targeting of Ywhaz and suppresses the mesangial hypertrophy in early diabetic nephropathy. FEBS Lett 586(1):20-6. [PubMed: 21827757]  [MGI Ref ID J:179943]

Zhang Z; Peng H; Chen J; Chen X; Han F; Xu X; He X; Yan N. 2009. MicroRNA-21 protects from mesangial cell proliferation induced by diabetic nephropathy in db/db mice. FEBS Lett 583(12):2009-14. [PubMed: 19450585]  [MGI Ref ID J:150000]

Zhao HJ; Wang S; Cheng H; Zhang MZ; Takahashi T; Fogo AB; Breyer MD; Harris RC. 2006. Endothelial nitric oxide synthase deficiency produces accelerated nephropathy in diabetic mice. J Am Soc Nephrol 17(10):2664-9. [PubMed: 16971655]  [MGI Ref ID J:135864]

Zhao R; Ren S; Moghadasain MH; Rempel JD; Shen GX. 2014. Involvement of fibrinolytic regulators in adhesion of monocytes to vascular endothelial cells induced by glycated LDL and to aorta from diabetic mice. J Leukoc Biol 95(6):941-9. [PubMed: 24496227]  [MGI Ref ID J:211922]

Zhao Y; Banerjee S; Dey N; LeJeune WS; Sarkar PS; Brobey R; Rosenblatt KP; Tilton RG; Choudhary S. 2011. Klotho depletion contributes to increased inflammation in kidney of the db/db mouse model of diabetes via RelA (serine)536 phosphorylation. Diabetes 60(7):1907-16. [PubMed: 21593200]  [MGI Ref ID J:186758]

Zhong X; Chung AC; Chen HY; Dong Y; Meng XM; Li R; Yang W; Hou FF; Lan HY. 2013. miR-21 is a key therapeutic target for renal injury in a mouse model of type 2 diabetes. Diabetologia 56(3):663-74. [PubMed: 23292313]  [MGI Ref ID J:194766]

Zhou L; Liu G; Jia Z; Yang KT; Sun Y; Kakizoe Y; Liu M; Zhou S; Chen R; Yang B; Yang T. 2013. Increased susceptibility of db/db mice to rosiglitazone-induced plasma volume expansion: role of dysregulation of renal water transporters. Am J Physiol Renal Physiol 305(10):F1491-7. [PubMed: 24005472]  [MGI Ref ID J:202994]

Zhou L; Liu M; Zhang J; Chen H; Dong LQ; Liu F. 2010. DsbA-L alleviates endoplasmic reticulum stress-induced adiponectin downregulation. Diabetes 59(11):2809-16. [PubMed: 20699416]  [MGI Ref ID J:169617]

Zhou T; He X; Cheng R; Zhang B; Zhang RR; Chen Y; Takahashi Y; Murray AR; Lee K; Gao G; Ma JX. 2012. Implication of dysregulation of the canonical wingless-type MMTV integration site (WNT) pathway in diabetic nephropathy. Diabetologia 55(1):255-66. [PubMed: 22016045]  [MGI Ref ID J:179020]

Zhou Y; Jia S; Wang C; Chen Z; Chi Y; Li J; Xu G; Guan Y; Yang J. 2013. FAM3A is a target gene of peroxisome proliferator-activated receptor gamma. Biochim Biophys Acta 1830(8):4160-70. [PubMed: 23562554]  [MGI Ref ID J:202406]

Zhou Y; Jiang L; Rui L. 2009. Identification of MUP1 as a regulator for glucose and lipid metabolism in mice. J Biol Chem 284(17):11152-9. [PubMed: 19258313]  [MGI Ref ID J:149849]

Zhou YP; Berggren PO; Grill V. 1996. A fatty acid-induced decrease in pyruvate dehydrogenase activity is an important determinant of beta-cell dysfunction in the obese diabetic db/db mouse. Diabetes 45(5):580-6. [PubMed: 8621007]  [MGI Ref ID J:32955]

Zimmermann C; Cederroth CR; Bourgoin L; Foti M; Nef S. 2012. Prevention of diabetes in db/db mice by dietary soy is independent of isoflavone levels. Endocrinology 153(11):5200-11. [PubMed: 22962258]  [MGI Ref ID J:191798]

Zykova SN; Jenssen TG; Berdal M; Olsen R; Myklebust R; Seljelid R. 2000. Altered cytokine and nitric oxide secretion in vitro by macrophages from diabetic type II-like db/db mice. Diabetes 49(9):1451-8. [PubMed: 10969828]  [MGI Ref ID J:107166]

Zyromski NJ; Mathur A; Pitt HA; Lu D; Gripe JT; Walker JJ; Yancey K; Wade TE; Swartz-Basile DA. 2008. A murine model of obesity implicates the adipokine milieu in the pathogenesis of severe acute pancreatitis. Am J Physiol Gastrointest Liver Physiol 295(3):G552-8. [PubMed: 18583460]  [MGI Ref ID J:141913]

de Luca C; Kowalski TJ; Zhang Y; Elmquist JK; Lee C; Kilimann MW; Ludwig T; Liu SM; Chua SC Jr. 2005. Complete rescue of obesity, diabetes, and infertility in db/db mice by neuron-specific LEPR-B transgenes. J Clin Invest 115(12):3484-93. [PubMed: 16284652]  [MGI Ref ID J:104582]

van Bilsen M; Daniels A; Brouwers O; Janssen BJ; Derks WJ; Brouns AE; Munts C; Schalkwijk CG; van der Vusse GJ; van Nieuwenhoven FA. 2014. Hypertension is a conditional factor for the development of cardiac hypertrophy in type 2 diabetic mice. PLoS One 9(1):e85078. [PubMed: 24416343]  [MGI Ref ID J:212203]

von Meyenn F; Porstmann T; Gasser E; Selevsek N; Schmidt A; Aebersold R; Stoffel M. 2013. Glucagon-induced acetylation of Foxa2 regulates hepatic lipid metabolism. Cell Metab 17(3):436-47. [PubMed: 23416070]  [MGI Ref ID J:198161]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX5
Room Number           AX8

Colony Maintenance

Breeding & HusbandrySince both males and females homozygous for Leprdb are sterile, the closely linked coat color mutation, m, has been incorporated into stocks for maintenance of the db mutation. Breeding is performed by mating repulsion double heterozygotes, Dock7m +/+ Leprdb, which presumably yield 1/4 diabetics (black, obese at weaning) for studies , 1/2 wild-type repulsion double heterozygotes (black, lean) for futher breeding, and 1/4 misty mice (grey, lean) that can be discarded. The risk of recombination between the Dock7m and Leprdb loci is only about 2%, recognizable in pups as young as 3 days old by absence of pigment in paws and tip of tail. Dietary restrictions can prolong life and carbohydrate-free, protein-enriched defined diets can diminish the significantly the severity of the disease.
Breeding Considerations This strain is a good breeder.
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Live Mice

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
4 weeks $82.65Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
5 weeks $86.40Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
6 weeks $90.20Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
7 weeks $93.95Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
8 weeks $93.95Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
9 weeks $100.70Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
10 weeks $104.50Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
4 weeks $82.65Female or MaleHomozygous for Dock7m  
5 weeks $86.40Female or MaleHomozygous for Dock7m  
6 weeks $90.20Female or MaleHomozygous for Dock7m  
7 weeks $93.95Female or MaleHomozygous for Dock7m  
8 weeks $97.65Female or MaleHomozygous for Dock7m  
9 weeks $100.70Female or MaleHomozygous for Dock7m  
10 weeks $104.50Female or MaleHomozygous for Dock7m  
4 weeks $113.25FemaleHomozygous for Leprdb  
$116.25MaleHomozygous for Leprdb  
5 weeks $116.95FemaleHomozygous for Leprdb  
$120.00MaleHomozygous for Leprdb  
6 weeks $120.70FemaleHomozygous for Leprdb  
$123.75MaleHomozygous for Leprdb  
7 weeks $124.50FemaleHomozygous for Leprdb  
$127.40MaleHomozygous for Leprdb  
8 weeks $124.50FemaleHomozygous for Leprdb  
$127.40MaleHomozygous for Leprdb  
9 weeks $128.15FemaleHomozygous for Leprdb  
$131.30MaleHomozygous for Leprdb  
10 weeks $131.90FemaleHomozygous for Leprdb  
$135.00MaleHomozygous for Leprdb  
Price per Pair (US dollars $)Pair Genotype
$180.40Heterozygous for Leprdb, Heterozygous for Dock7m x Heterozygous for Leprdb, Heterozygous for Dock7m  

Standard Supply

Level 2. Up to 100 mice. Larger quantities or custom orders arranged upon request.

Supply Notes

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
4 weeks $107.50Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
5 weeks $112.40Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
6 weeks $117.30Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
7 weeks $122.20Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
8 weeks $122.20Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
9 weeks $131.00Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
10 weeks $135.90Female or MaleHeterozygous for Leprdb, Heterozygous for Dock7m  
4 weeks $107.50Female or MaleHomozygous for Dock7m  
5 weeks $112.40Female or MaleHomozygous for Dock7m  
6 weeks $117.30Female or MaleHomozygous for Dock7m  
7 weeks $122.20Female or MaleHomozygous for Dock7m  
8 weeks $127.00Female or MaleHomozygous for Dock7m  
9 weeks $131.00Female or MaleHomozygous for Dock7m  
10 weeks $135.90Female or MaleHomozygous for Dock7m  
4 weeks $147.30FemaleHomozygous for Leprdb  
$151.20MaleHomozygous for Leprdb  
5 weeks $152.10FemaleHomozygous for Leprdb  
$156.00MaleHomozygous for Leprdb  
6 weeks $157.00FemaleHomozygous for Leprdb  
$160.90MaleHomozygous for Leprdb  
7 weeks $161.90FemaleHomozygous for Leprdb  
$165.70MaleHomozygous for Leprdb  
8 weeks $161.90FemaleHomozygous for Leprdb  
$165.70MaleHomozygous for Leprdb  
9 weeks $166.60FemaleHomozygous for Leprdb  
$170.70MaleHomozygous for Leprdb  
10 weeks $171.50FemaleHomozygous for Leprdb  
$175.50MaleHomozygous for Leprdb  
Price per Pair (US dollars $)Pair Genotype
$234.60Heterozygous for Leprdb, Heterozygous for Dock7m x Heterozygous for Leprdb, Heterozygous for Dock7m  

Standard Supply

Level 2. Up to 100 mice. Larger quantities or custom orders arranged upon request.

Supply Notes

  • Mice are not available until four weeks of age.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
  • This strain is available from some international Charles River (CR) breeding facilities in Japan and/or Europe. For more information, see the Worldwide Distributor List for JAX® Mice.
View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Level 2. Up to 100 mice. Larger quantities or custom orders arranged upon request.

Control Information

  Control
   Dock7m +/+ Leprdb (Heterozygote from the colony)
   Dock7m +/Dock7m + from the colony
   000662 C57BLKS/J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Important Note

This strain is maintained with Dock7m and Leprdb in repulsion. Although these genes are tightly linked, there is a small possibility of recombination. The heterozygotes we distribute are presumed to be non-recombinant, but are untested.

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
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Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
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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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