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Level 2

Common Names: B6 db;    
Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around 3 to 4 weeks of age with elevations of plasma insulin beginning at 10 to 14 days and of blood sugar at four to eight weeks. Affected mice are polyphagic, polydipsic, and polyuric.


Strain Information

Former Names B6.BKS-Leprdb    (Changed: 23-FEB-10 )
B6.Cg-Dock7m +/+ Leprdb/J    (Changed: 14-MAY-09 )
B6.Cg-m +/+ Leprdb/J    (Changed: 28-APR-09 )
Type Congenic; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Mating SystemHomozygous for Leprdb (ovarian transplant) x Heterozygous         (Female x Male)   02-JUL-14
Breeding Considerations This strain is a good breeder.
Specieslaboratory mouse
Background Strain C57BL/6J
Donor Strain C57BLKS
H2 Haplotypeb
GenerationN1F19 (05-AUG-14)
Generation Definitions

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

Important Note
In the spring of 2009, The Jackson Laboratory eliminated the allele misty (m) from the 000697 colony. Misty was bred out at generation 86. It is distributed as B6.D2(BKS)-Dock7m/J (009659).

Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around 3 to 4 weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at four to eight weeks. Affected mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. On the C57BL/6 background there is compensatory hyperplasia of the islet B cells, and continued hyperinsulinemia throughout an 18- to 20-month life span. Wound healing is delayed and metabolic efficiency is increased. 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.

For Heterozygous mice only, this strain ships with a JAXTagTM affixed. Learn more about JAXTagTM.

The spontaneous autosomal recessive mutation diabetes, db was discovered at The Jackson Laboratory, Bar Harbor, ME in 1966 on the inbred strain C57BLKS/J. Formerly known as db, after cloning it became Leprdb. Additional backgrounds available: C57BLKS/J-Dock7m +/+ Leprdb (000642), C57BL/6J-Dock7m Leprdb/+ + (000699), C57BLKS/J-Dock7m Leprdb/+ + (000700).

Control Information

   Heterozygote from the colony
   000664 C57BL/6J
  Considerations for Choosing Controls

Related 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
019377   B6.129P2(Cg)-Leprtm1.1Rck/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     (10 strains)

Additional Web Information

Comparison of widely used JAX® Mice for type 2 diabetes and obesity


Phenotype Information

View Phenotypic Data

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
- 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


        B6.Cg-Dock7m +/+ Leprdb/J
  • growth/size/body region 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)


        involves: C57BL/6
  • skeleton phenotype
  • abnormal skeleton development
    • rate of new bone formation increased at both 3 and 6 months   (MGI Ref ID J:60001)
    • abnormal osteoclast differentiation
      • increased numbers of osteoclasts   (MGI Ref ID J:60001)
  • increased bone volume
    • 3 fold increase in bone volume   (MGI Ref ID J:60001)
  • hematopoietic system phenotype
  • abnormal osteoclast differentiation
    • increased numbers of osteoclasts   (MGI Ref ID J:60001)
  • immune system phenotype
  • abnormal osteoclast differentiation
    • increased numbers of osteoclasts   (MGI Ref ID J:60001)
  • cellular phenotype
  • abnormal osteoclast differentiation
    • increased numbers of osteoclasts   (MGI Ref ID J:60001)


  • 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)

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


        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 region phenotype
  • increased body weight
    • slight but significant increase in body weight compared to wild-type mice   (MGI Ref ID J:82334)


        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 region 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)


        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)


        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)
        • at 12 weeks   (MGI Ref ID J:210493)
    • 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 region 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)
  • endocrine/exocrine gland phenotype
  • abnormal pancreatic beta cell physiology
    • beta cells exhibit DNA damage unlike control cells   (MGI Ref ID J:210493)


  • growth/size/body region 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)


        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 region 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)


        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)


        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)


        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 region 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)


        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)
View Research Applications

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

Diabetes and Obesity Research
Type 2 Diabetes (NIDDM)

Internal/Organ Research
Wound Healing

Leprdb related

Diabetes and Obesity Research
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 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 Information

Genotyping Protocols

Lepr db, End Point Analysis
Leprdb, Restriction Enzyme Digest

Helpful Links

Genotyping resources and troubleshooting


References provided by MGI

Selected Reference(s)

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]

Additional References

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]

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]

Konstantinides S; Schafer K; Koschnick S; Loskutoff DJ. 2001. Leptin-dependent platelet aggregation and arterial thrombosis suggests a mechanism for atherothrombotic disease in obesity. J Clin Invest 108(10):1533-40. [PubMed: 11714745]  [MGI Ref ID J:109859]

Liu K; Xu L; Szalkowski D; Li Z; Ding V; Kwei G; Huskey S; Moller DE; Heck JV; Zhang BB; Jones AB. 2000. Discovery of a potent, highly selective, and orally efficacious small-molecule activator of the insulin receptor. J Med Chem 43(19):3487-94. [PubMed: 11000003]  [MGI Ref ID J:109888]

Norido F; Canella R; Zanoni R; Gorio A. 1984. Development of diabetic neuropathy in the C57BL/Ks (db/db) mouse and its treatment with gangliosides. Exp Neurol 83(2):221-32. [PubMed: 6692864]  [MGI Ref ID J:7294]

Petkov PM; Cassell MA; Sargent EE; Donnelly CJ; Robinson P; Crew V; Asquith S; Haar RV; Wiles MV. 2004. Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse. Genomics 83(5):902-11. [PubMed: 15081119]  [MGI Ref ID J:89298]

Shimoni Y. 2001. Inhibition of the formation or action of angiotensin II reverses attenuated K+ currents in type 1 and type 2 diabetes. J Physiol 537(Pt 1):83-92. [PubMed: 11711563]  [MGI Ref ID J:109861]

Witthuhn BA; Bernlohr DA. 2001. Upregulation of bone morphogenetic protein GDF-3/Vgr-2 expression in adipose tissue of FABP4/aP2 null mice. Cytokine 14(3):129-35. [PubMed: 11396990]  [MGI Ref ID J:109875]

Leprdb related

Aasum E; Hafstad AD; Severson DL; Larsen TS. 2003. Age-dependent changes in metabolism, contractile function, and ischemic sensitivity in hearts from db/db mice. Diabetes 52(2):434-41. [PubMed: 12540618]  [MGI Ref ID J:107138]

Abe H; Uchida T; Hara A; Mizukami H; Komiya K; Koike M; Shigihara N; Toyofuku Y; Ogihara T; Uchiyama Y; Yagihashi S; Fujitani Y; Watada H. 2013. Exendin-4 improves beta-cell function in autophagy-deficient beta-cells. Endocrinology 154(12):4512-24. [PubMed: 24105478]  [MGI Ref ID J:205147]

Absood A; Gandomani B; Zaki A; Nasta V; Michail A; Habib PM; Hodish I. 2013. Insulin therapy for pre-hyperglycemic beta-cell endoplasmic reticulum crowding. PLoS One 8(2):e54351. [PubMed: 23408938]  [MGI Ref ID J:198317]

Adkison DL; Sundberg JP. 1991. Lipomatous hamartomas and choristomas in inbred laboratory mice. Vet Pathol 28(4):305-12. [PubMed: 1949510]  [MGI Ref ID J:2714]

Agarwal P; Srivastava R; Srivastava AK; Ali S; Datta M. 2013. miR-135a targets IRS2 and regulates insulin signaling and glucose uptake in the diabetic gastrocnemius skeletal muscle. Biochim Biophys Acta 1832(8):1294-303. [PubMed: 23579070]  [MGI Ref ID J:202403]

Ahima RS; Prabakaran D; Flier JS. 1998. Postnatal leptin surge and regulation of circadian rhythm of leptin by feeding. Implications for energy homeostasis and neuroendocrine function. J Clin Invest 101(5):1020-7. [PubMed: 9486972]  [MGI Ref ID J:118976]

Akamatsu Y; Nishijima Y; Lee CC; Yang SY; Shi L; An L; Wang RK; Tominaga T; Liu J. 2015. Impaired Leptomeningeal Collateral Flow Contributes to the Poor Outcome following Experimental Stroke in the Type 2 Diabetic Mice. J Neurosci 35(9):3851-64. [PubMed: 25740515]  [MGI Ref ID J:219934]

Akasaka Y; Tsunoda M; Ogata T; Ide T; Murakami K. 2010. Direct evidence for leptin-induced lipid oxidation independent of long-form leptin receptor. Biochim Biophys Acta 1801(10):1115-22. [PubMed: 20601111]  [MGI Ref ID J:165456]

Akpinar P; Kuwajima S; Krutzfeldt J; Stoffel M. 2005. Tmem27: a cleaved and shed plasma membrane protein that stimulates pancreatic beta cell proliferation. Cell Metab 2(6):385-97. [PubMed: 16330324]  [MGI Ref ID J:129667]

Al-Mashat HA; Kandru S; Liu R; Behl Y; Desta T; Graves DT. 2006. Diabetes enhances mRNA levels of proapoptotic genes and caspase activity, which contribute to impaired healing. Diabetes 55(2):487-95. [PubMed: 16443785]  [MGI Ref ID J:106866]

Alberts P; Nilsson C; Selen G; Engblom LO; Edling NH; Norling S; Klingstrom G; Larsson C; Forsgren M; Ashkzari M; Nilsson CE; Fiedler M; Bergqvist E; Ohman B; Bjorkstrand E; Abrahmsen LB. 2003. Selective inhibition of 11 beta-hydroxysteroid dehydrogenase type 1 improves hepatic insulin sensitivity in hyperglycemic mice strains. Endocrinology 144(11):4755-62. [PubMed: 12960099]  [MGI Ref ID J:87239]

Algamas-Dimantov A; Davidovsky D; Ben-Ari J; Kang JX; Peri I; Hertz R; Bar-Tana J; Schwartz B. 2012. Amelioration of diabesity-induced colorectal ontogenesis by omega-3 fatty acids in mice. J Lipid Res 53(6):1056-70. [PubMed: 22357704]  [MGI Ref ID J:184929]

Ali MI; Ketsawatsomkron P; Belin de Chantemele EJ; Mintz JD; Muta K; Salet C; Black SM; Tremblay ML; Fulton DJ; Marrero MB; Stepp DW. 2009. Deletion of protein tyrosine phosphatase 1b improves peripheral insulin resistance and vascular function in obese, leptin-resistant mice via reduced oxidant tone. Circ Res 105(10):1013-22. [PubMed: 19797171]  [MGI Ref ID J:169952]

Alipio Z; Liao W; Roemer EJ; Waner M; Fink LM; Ward DC; Ma Y. 2010. Reversal of hyperglycemia in diabetic mouse models using induced-pluripotent stem (iPS)-derived pancreatic beta-like cells. Proc Natl Acad Sci U S A 107(30):13426-31. [PubMed: 20616080]  [MGI Ref ID J:162403]

Allen RJ Jr; Soares MA; Haberman ID; Szpalski C; Schachar J; Lin CD; Nguyen PD; Saadeh PB; Warren SM. 2014. Combination therapy accelerates diabetic wound closure. PLoS One 9(3):e92667. [PubMed: 24651576]  [MGI Ref ID J:215069]

Alonso-Magdalena P; Ropero AB; Garcia-Arevalo M; Soriano S; Quesada I; Muhammed SJ; Salehi A; Gustafsson JA; Nadal A. 2013. Antidiabetic actions of an estrogen receptor beta selective agonist. Diabetes 62(6):2015-25. [PubMed: 23349481]  [MGI Ref ID J:208572]

Altarejos JY; Goebel N; Conkright MD; Inoue H; Xie J; Arias CM; Sawchenko PE; Montminy M. 2008. The Creb1 coactivator Crtc1 is required for energy balance and fertility. Nat Med 14(10):1112-7. [PubMed: 18758446]  [MGI Ref ID J:142448]

Altomonte J; Cong L; Harbaran S; Richter A; Xu J; Meseck M; Dong HH. 2004. Foxo1 mediates insulin action on apoC-III and triglyceride metabolism. J Clin Invest 114(10):1493-503. [PubMed: 15546000]  [MGI Ref ID J:94423]

Amin A; Choi SK; Galan M; Kassan M; Partyka M; Kadowitz P; Henrion D; Trebak M; Belmadani S; Matrougui K. 2012. Chronic inhibition of endoplasmic reticulum stress and inflammation prevents ischaemia-induced vascular pathology in type II diabetic mice. J Pathol 227(2):165-74. [PubMed: 22081301]  [MGI Ref ID J:183318]

Amin AH; Abd Elmageed ZY; Nair D; Partyka MI; Kadowitz PJ; Belmadani S; Matrougui K. 2010. Modified multipotent stromal cells with epidermal growth factor restore vasculogenesis and blood flow in ischemic hind-limb of type II diabetic mice. Lab Invest 90(7):985-96. [PubMed: 20440273]  [MGI Ref ID J:162143]

Anzawa R; Bernard M; Tamareille S; Baetz D; Confort-Gouny S; Gascard JP; Cozzone P; Feuvray D. 2006. Intracellular sodium increase and susceptibility to ischaemia in hearts from type 2 diabetic db/db mice. Diabetologia 49(3):598-606. [PubMed: 16425033]  [MGI Ref ID J:107891]

Aoki K; Saito T; Satoh S; Mukasa K; Kaneshiro M; Kawasaki S; Okamura A; Sekihara H. 1999. Dehydroepiandrosterone suppresses the elevated hepatic glucose-6-phosphatase and fructose-1,6-bisphosphatase activities in C57BL/Ksj-db/db mice: comparison with troglitazone. Diabetes 48(8):1579-85. [PubMed: 10426376]  [MGI Ref ID J:56421]

Ardestani A; Sauter NS; Paroni F; Dharmadhikari G; Cho JH; Lupi R; Marchetti P; Oberholzer J; Conte JK; Maedler K. 2011. Neutralizing Interleukin-1{beta} (IL-1{beta}) Induces {beta}-Cell Survival by Maintaining PDX1 Protein Nuclear Localization. J Biol Chem 286(19):17144-55. [PubMed: 21393239]  [MGI Ref ID J:172695]

Ariyasu H; Takaya K; Hosoda H; Iwakura H; Ebihara K; Mori K; Ogawa Y; Hosoda K; Akamizu T; Kojima M; Kangawa K; Nakao K. 2002. Delayed short-term secretory regulation of ghrelin in obese animals: evidenced by a specific RIA for the active form of ghrelin. Endocrinology 143(9):3341-50. [PubMed: 12193546]  [MGI Ref ID J:81463]

Arounleut P; Bowser M; Upadhyay S; Shi XM; Fulzele S; Johnson MH; Stranahan AM; Hill WD; Isales CM; Hamrick MW. 2013. Absence of functional leptin receptor isoforms in the POUND (Lepr(db/lb)) mouse is associated with muscle atrophy and altered myoblast proliferation and differentiation. PLoS One 8(8):e72330. [PubMed: 23967295]  [MGI Ref ID J:204438]

Asahara S; Matsuda T; Kido Y; Kasuga M. 2009. Increased ribosomal biogenesis induces pancreatic beta cell failure in mice model of type 2 diabetes. Biochem Biophys Res Commun 381(3):367-71. [PubMed: 19309774]  [MGI Ref ID J:147192]

Asai J; Takenaka H; Hirakawa S; Sakabe J; Hagura A; Kishimoto S; Maruyama K; Kajiya K; Kinoshita S; Tokura Y; Katoh N. 2012. Topical simvastatin accelerates wound healing in diabetes by enhancing angiogenesis and lymphangiogenesis. Am J Pathol 181(6):2217-24. [PubMed: 23138019]  [MGI Ref ID J:192238]

Asai J; Takenaka H; Kusano KF; Ii M; Luedemann C; Curry C; Eaton E; Iwakura A; Tsutsumi Y; Hamada H; Kishimoto S; Thorne T; Kishore R; Losordo DW. 2006. Topical sonic hedgehog gene therapy accelerates wound healing in diabetes by enhancing endothelial progenitor cell-mediated microvascular remodeling. Circulation 113(20):2413-24. [PubMed: 16702471]  [MGI Ref ID J:122447]

Atkinson RD; Coenen KR; Plummer MR; Gruen ML; Hasty AH. 2008. Macrophage-derived apolipoprotein E ameliorates dyslipidemia and atherosclerosis in obese apolipoprotein E-deficient mice. Am J Physiol Endocrinol Metab 294(2):E284-90. [PubMed: 18029445]  [MGI Ref ID J:133332]

Awazawa M; Futami T; Sakada M; Kaneko K; Ohsugi M; Nakaya K; Terai A; Suzuki R; Koike M; Uchiyama Y; Kadowaki T; Ueki K. 2014. Deregulation of pancreas-specific oxidoreductin ERO1beta in the pathogenesis of diabetes mellitus. Mol Cell Biol 34(7):1290-9. [PubMed: 24469402]  [MGI Ref ID J:213523]

Awazawa M; Ueki K; Inabe K; Yamauchi T; Kaneko K; Okazaki Y; Bardeesy N; Ohnishi S; Nagai R; Kadowaki T. 2009. Adiponectin suppresses hepatic SREBP1c expression in an AdipoR1/LKB1/AMPK dependent pathway. Biochem Biophys Res Commun 382(1):51-6. [PubMed: 19254698]  [MGI Ref ID J:147384]

Awazawa M; Ueki K; Inabe K; Yamauchi T; Kubota N; Kaneko K; Kobayashi M; Iwane A; Sasako T; Okazaki Y; Ohsugi M; Takamoto I; Yamashita S; Asahara H; Akira S; Kasuga M; Kadowaki T. 2011. Adiponectin enhances insulin sensitivity by increasing hepatic IRS-2 expression via a macrophage-derived IL-6-dependent pathway. Cell Metab 13(4):401-12. [PubMed: 21459325]  [MGI Ref ID J:172246]

Baba M; Wada J; Eguchi J; Hashimoto I; Okada T; Yasuhara A; Shikata K; Kanwar YS; Makino H. 2005. Galectin-9 inhibits glomerular hypertrophy in db/db diabetic mice via cell-cycle-dependent mechanisms. J Am Soc Nephrol 16(11):3222-34. [PubMed: 16177004]  [MGI Ref ID J:116853]

Bagi Z; Erdei N; Toth A; Li W; Hintze TH; Koller A; Kaley G. 2005. Type 2 diabetic mice have increased arteriolar tone and blood pressure: enhanced release of COX-2-derived constrictor prostaglandins. Arterioscler Thromb Vasc Biol 25(8):1610-6. [PubMed: 15947245]  [MGI Ref ID J:114331]

Bagi Z; Koller A; Kaley G. 2004. PPARgamma activation, by reducing oxidative stress, increases NO bioavailability in coronary arterioles of mice with Type 2 diabetes. Am J Physiol Heart Circ Physiol 286(2):H742-8. [PubMed: 14551045]  [MGI Ref ID J:87610]

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]

Bailly-Maitre B; Belgardt BF; Jordan SD; Coornaert B; von Freyend MJ; Kleinridders A; Mauer J; Cuddy M; Kress CL; Willmes D; Essig M; Hampel B; Protzer U; Reed JC; Bruning JC. 2010. Hepatic Bax inhibitor-1 inhibits IRE1alpha and protects from obesity-associated insulin resistance and glucose intolerance. J Biol Chem 285(9):6198-207. [PubMed: 19996103]  [MGI Ref ID J:159765]

Balland E; Dam J; Langlet F; Caron E; Steculorum S; Messina A; Rasika S; Falluel-Morel A; Anouar Y; Dehouck B; Trinquet E; Jockers R; Bouret SG; Prevot V. 2014. Hypothalamic tanycytes are an ERK-gated conduit for leptin into the brain. Cell Metab 19(2):293-301. [PubMed: 24506870]  [MGI Ref ID J:210650]

Balthasar N; Coppari R; McMinn J; Liu SM; Lee CE; Tang V; Kenny CD; McGovern RA; Chua SC Jr; Elmquist JK; Lowell BB. 2004. Leptin receptor signaling in POMC neurons is required for normal body weight homeostasis. Neuron 42(6):983-91. [PubMed: 15207242]  [MGI Ref ID J:106354]

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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]

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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]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX1
Room Number           RB07

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice are bred as heterozygotes. Females homozygous for the mutation are infertile and males exhibit a reduced ability to mate.
Mating SystemHomozygous for Leprdb (ovarian transplant) x Heterozygous         (Female x Male)   02-JUL-14
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 $106.90Female or MaleHeterozygous for Leprdb  
5 weeks $106.90Female or MaleHeterozygous for Leprdb  
6 weeks $111.21Female or MaleHeterozygous for Leprdb  
7 weeks $115.53Female or MaleHeterozygous for Leprdb  
8 weeks $119.84Female or MaleHeterozygous for Leprdb  
9 weeks $124.15Female or MaleHeterozygous for Leprdb  
10 weeks $128.46Female or MaleHeterozygous for Leprdb  
4 weeks $139.40FemaleHomozygous for Leprdb  
$142.40MaleHomozygous for Leprdb  
5 weeks $139.40FemaleHomozygous for Leprdb  
$142.40MaleHomozygous for Leprdb  
6 weeks $143.71FemaleHomozygous for Leprdb  
$146.71MaleHomozygous for Leprdb  
7 weeks $148.03FemaleHomozygous for Leprdb  
$151.03MaleHomozygous for Leprdb  
8 weeks $152.34FemaleHomozygous for Leprdb  
$155.34MaleHomozygous for Leprdb  
9 weeks $156.65FemaleHomozygous for Leprdb  
$159.65MaleHomozygous for Leprdb  
10 weeks $160.96FemaleHomozygous for Leprdb  
$163.96MaleHomozygous for Leprdb  

Standard Supply

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

Supply Notes

  • This strain is available from both the Bar Harbor, Maine and Sacramento, Calif. facilities.
  • For Heterozygous mice only, this strain ships with a JAXTagTM affixed. Learn more about JAXTagTM.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
4 weeks $139.00Female or MaleHeterozygous for Leprdb  
5 weeks $139.00Female or MaleHeterozygous for Leprdb  
6 weeks $144.60Female or MaleHeterozygous for Leprdb  
7 weeks $150.20Female or MaleHeterozygous for Leprdb  
8 weeks $155.80Female or MaleHeterozygous for Leprdb  
9 weeks $161.40Female or MaleHeterozygous for Leprdb  
10 weeks $167.10Female or MaleHeterozygous for Leprdb  
4 weeks $181.30FemaleHomozygous for Leprdb  
$185.20MaleHomozygous for Leprdb  
5 weeks $181.30FemaleHomozygous for Leprdb  
$185.20MaleHomozygous for Leprdb  
6 weeks $186.90FemaleHomozygous for Leprdb  
$190.80MaleHomozygous for Leprdb  
7 weeks $192.50FemaleHomozygous for Leprdb  
$196.40MaleHomozygous for Leprdb  
8 weeks $198.10FemaleHomozygous for Leprdb  
$202.00MaleHomozygous for Leprdb  
9 weeks $203.70FemaleHomozygous for Leprdb  
$207.60MaleHomozygous for Leprdb  
10 weeks $209.30FemaleHomozygous for Leprdb  
$213.20MaleHomozygous for Leprdb  

Standard Supply

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

Supply Notes

  • For Heterozygous mice only, this strain ships with a JAXTagTM affixed. Learn more about JAXTagTM.
  • Strains that require genotyping are only offered at five weeks of age and older. The time required for sample collection, assay, reporting, and completion of USDA documentation required for international purchases make distribution of younger mice prohibitive. Mice at a precise age in days, littermates and retired breeders are also available. Mice older than 10 weeks of age can be requested by contacting JAX® Mice & Services.
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

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

Important Note

In the spring of 2009, The Jackson Laboratory eliminated the allele misty (m) from the 000697 colony. Misty was bred out at generation 86. It is distributed as B6.D2(BKS)-Dock7m/J (009659).

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
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Terms of Use

Terms of Use

General Terms and Conditions

Contact information

General inquiries regarding Terms of Use

Contracts Administration


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


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.