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Strain Name:

B6.Cg-m +/+ Leprdb/J

Stock Number:

000697

Availability:

Level 3

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General Terms and Conditions

Genes & Alleles   Lepr;   Leprdb;   m;

Product Information

Strain Details

Type JAX® GEMM® Strain - Congenic
Additional information on JAX® GEMM® Strains.
Type JAX® GEMM® Strain - Mutant Strain
Specieslaboratory mouse
Background Strain C57BL/6J
Donor Strain Leprdb, C57BLKS; m, DBA/J
H2 Haplotypeb
GenerationN5F84 (11-JAN-08)

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

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

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

Important Note
This strain is maintained with m 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.

Strain Description
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 4 to 8 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. Because of the sterility of Leprdb homozygotes, misty has been incorporated into stocks for maintenance of the diabetes mutation. The repulsion double heterozygote (m +/+ Leprdb) facilitates identification of heterozygotes for breeding, while the coupling double heterozygote, (m Leprdb/+ +, Stock No. 000699) 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 m/m 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 m/m mice than from wildtype controls. Between two and five weeks of age, m/m 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, there is increased bleed time and reduced platelet AD levels in m/m homozygotes. (Woolley, 1941 and 1945; Truett et al., 1998; Sviderskaya et al., 1998.)

Strain Development
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-m +/+ Leprdb (000642), C57BL/6J-m Leprdb/+ + (000699), C57BLKS/J-m Leprdb/+ + (000700).

Related Disease (OMIM) Terms

Diabetes Mellitus, Noninsulin-Dependent; NIDDM
Mammalian Phenotype Terms assigned by genotype

Leprdb/Lepr+

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

Leprdb/Leprdb

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

m/m

        B6.D2(Cg)-m
  • adipose tissue phenotype
  • abnormal brown adipose tissue amount (MGI Ref ID J:45425)
    • appeared to be completely absent in neonatal mice
  • decreased white adipose tissue amount (MGI Ref ID J:48831)
    • mice have 21% less inguinal adipose mass
  • growth/size phenotype
  • decreased body length (MGI Ref ID J:48831)
    • mutants are 8% shorter
  • decreased body weight (MGI Ref ID J:48831)
    • mutants weigh 15% less
  • hematopoietic system phenotype
  • platelet storage pool deficiency (MGI Ref ID J:45425)
    • platelet count, platelet serotonin and ATP levels normal
    • platelet ADP levels low
  • homeostasis/metabolism phenotype
  • increased bleeding time (MGI Ref ID J:45425)
  • platelet storage pool deficiency (MGI Ref ID J:45425)
    • platelet count, platelet serotonin and ATP levels normal
    • platelet ADP levels low

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

Leprdb/Lepr+

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

Leprdb/Lepr+

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

Leprdb/Leprdb

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

Leprdb/Leprdb

        C57BLKS/J
  • behavior/neurological phenotype
  • polyphagia (MGI Ref ID J:96047)
  • digestive/alimentary phenotype
  • abnormal islet of Langerhans morphology (MGI Ref ID J:96047)
    • islet mass and density are significantly increased compared to wild type mice
    • abnormal pancreatic beta cell morphology (MGI Ref ID J:96047)
      • individual beta cell size is increased
  • endocrine/exocrine gland phenotype
  • abnormal islet of Langerhans morphology (MGI Ref ID J:96047)
    • islet mass and density are significantly increased compared to wild type mice
    • abnormal pancreatic beta cell morphology (MGI Ref ID J:96047)
      • individual beta cell size is increased
  • growth/size phenotype
  • increased body weight (MGI Ref ID J:106597)
    • overweight by 4 weeks of age
  • homeostasis/metabolism phenotype
  • abnormal glucose homeostasis (MGI Ref ID J:107138)
    • diabetic phenotype appears earlier in males than in females
    • hyperglycemia (MGI Ref ID J:104790)
      • by 8 weeks
    • increased circulating insulin level (MGI Ref ID J:104790)
      • hyperinsulinemia by 8 weeks
  • abnormal metabolism (MGI Ref ID J:107138)
    • carbohydrate oxidation becomes reduced
    • palmitate oxidation is elevated
  • altered response to myocardial infarction (MGI Ref ID J:104790)
    • 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
  • decreased body temperature (MGI Ref ID J:96047)
  • hyperlipidemia (MGI Ref ID J:96047)
  • incleased glycosylated hemoglobin level (MGI Ref ID J:104790)
    • significant increase in the percentage of plasma glycosylated hemoglobin
  • increased circulating free fatty acid level (MGI Ref ID J:106871)
  • cardiovascular system phenotype
  • abnormal cardiac muscle morphology (MGI Ref ID J:107138)
    • myocardial triacylglycerol content 2X that of controls at 10-18 weeks of age
  • 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
    • abnormal blood circulation (MGI Ref ID J:107138)
      • reduced aortic flow
      • cardiac ischemia (MGI Ref ID J:107138)
        • reduced recovery of mechanical function after 13 minutes of ischemia and reperfusion
      • decreased cardiac output (MGI Ref ID J:107138)
        • cardiac output is reduced in fatty acid perfused hearts
    • altered response to myocardial infarction (MGI Ref ID J:104790)
      • 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
    • decreased cardiac muscle contractility (MGI Ref ID J:106871)
      • 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
    • decreased heart rate (MGI Ref ID J:107138)
      • intrinsic heart rates are reduced at all workloads
    • decreased systolic blood pressure (MGI Ref ID J:107138)
      • decreased peak systolic pressure
      • decreased peak systolic pressure X cardiac output
      • decreased peak systolic pressure X heart rate
    • increased left ventricle diastolic pressure (MGI Ref ID J:106871)
      • 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
  • hematopoietic system phenotype
  • incleased glycosylated hemoglobin level (MGI Ref ID J:104790)
    • significant increase in the percentage of plasma glycosylated hemoglobin
  • life span-post-weaning/aging
  • abnormal induced morbidity/mortality (MGI Ref ID J:104790)
    • 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
    • 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
  • cellular phenotype
  • abnormal aerobic energy metabolism (MGI Ref ID J:106871)
    • elevation of fatty acids in perfused hearts causes an increase in fatty acid oxidation combined with a reduction in glucose oxidation rates
    • state 3 respiration is elevated in cardiac mitochondria incubated with palmitoyl-carnitine but not with pyruvate
  • muscle phenotype
  • abnormal cardiac muscle morphology (MGI Ref ID J:107138)
    • myocardial triacylglycerol content 2X that of controls at 10-18 weeks of age
  • decreased cardiac muscle contractility (MGI Ref ID J:106871)
    • 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
  • increased vascular smooth muscle contraction (MGI Ref ID J:106597)
    • hypercontractility of smooth muscle in aortic strips due to either phenylephrine or serotonin
    • hypercontractility corrollated with the levels of obesity, hyperglycemia, and hyperinsulinemia
    • maximal contractions increase with age rather than decrease as in controls

Leprdb/Leprdb

        FVB.BKS-Leprdb
  • growth/size phenotype
  • obese (MGI Ref ID J:78850)
    • mice of both sexes are obese
  • homeostasis/metabolism phenotype
  • abnormal circulating glucose level (MGI Ref ID J:78850)
    • after a 2-day fast on refeeding with carbohydrate-free diet, female obese mice show a rise in glucose
    • hyperglycemia (MGI Ref ID J:78850)
      • obese mice have a prolonged period of hyperglycemia compared to obese B6.BKS-Leprdb mice where glucose levels rarely exceed 250 mg/dl
      • fasting mice are hyperglycemic at 3 months of age, while obese B6.BKS-Leprdb fasted mice are euglycemic
      • 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)
  • impaired glucose tolerance (MGI Ref ID J:78850)
    • 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
    • obese mice show a rapid increase of blood glucose above 400 mg/dl with diminished rate of glucose clearance
  • increased circulating insulin level (MGI Ref ID J:78850)
    • 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)
  • insulin resistance (MGI Ref ID J:78850)
    • 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
    • at a dose of 3U/kg 6-week old mice show a diminished response to insulin
    • circulating insulin levels in the fed state show that obese mice have exteme insulin resistance
  • endocrine/exocrine gland phenotype
  • abnormal islet of Langerhans morphology (MGI Ref ID J:78850)
    • some islets in obese mice have more than 1000 cells per cross section; such islets are absent in lean mice
    • increased pancreatic beta cell number (MGI Ref ID J:78850)
      • 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
  • digestive/alimentary phenotype
  • abnormal islet of Langerhans morphology (MGI Ref ID J:78850)
    • some islets in obese mice have more than 1000 cells per cross section; such islets are absent in lean mice
    • increased pancreatic beta cell number (MGI Ref ID J:78850)
      • 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
  • renal/urinary system phenotype
  • abnormal renal glomerulus morphology (MGI Ref ID J:78850)
    • 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

Leprdb/Leprdb

        BKS.Cg-m +/+ Leprdb/J
  • homeostasis/metabolism phenotype
  • abnormal circulating glucose level (MGI Ref ID J:43162)
    • decreased circulating glucose level (MGI Ref ID J:43162)
      • brain derived neurotrophic factor (BDNF) causes a drop in blood glucose relative to controls 8 weeks after treatment
      • affect of BDNF on blood glucose becomes progressively less as mice age
      • neurotrophin 3 also causes a drop in blood glucose but the glucose levels return to normal by 24 hours after treatment
      • glucose levels are reduced at all times tested when mice are placed on feeding restriction during the dark phase
    • increased circulating glucose level (MGI Ref ID J:6323)
      • blood glucose shows a progressive increase from 5 through 33 weeks
  • abnormal circulating lipid level (MGI Ref ID J:18161)
    • 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
    • abnormal circulating cholesterol level (MGI Ref ID J:18161)
      • increased circulating cholesterol level (MGI Ref ID J:18161)
        • fasting plasma total cholesterol concentration is increased 2 fold over controls
        • 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 (MGI Ref ID J:91813)
      • triglyceride levels are reduced at all times tested when mice are placed on feeding restriction during the dark phase
    • increased circulating triglyceride level (MGI Ref ID J:18161)
      • triglyceride levels are elevated 1.5- to 2-fold
  • decreased albumin excretion (MGI Ref ID J:82491)
    • 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)
  • decreased circulating insulin level (MGI Ref ID J:43162)
    • BDNF causes a 50% reduction in plasma insulin relative to controls
    • morning insulin levels lowered when feeding is restricted during the dark phase
  • improved glucose tolerance (MGI Ref ID J:43162)
    • BDNF treatment causes a lower blood glucose level response in a glucose tolerance test
  • growth/size phenotype
  • obese (MGI Ref ID J:6323)
    • become progressively obese starting at 5 weeks of age
    • weight reaches 2.5X that of control mice by 3 months of age
  • weight loss (MGI Ref ID J:91813)
    • body weight drops after 6 days on feeding restriction during the dark phase
  • renal/urinary system phenotype
  • decreased albumin excretion (MGI Ref ID J:82491)
    • 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)
  • increased creatinine clearance (MGI Ref ID J:82491)
    • 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)
  • nervous system phenotype
  • abnormal CNS synaptic transmission (MGI Ref ID J:109401)
    • absent long term depression (MGI Ref ID J:109401)
      • CA1 hippocampal slices indicate no long term depression on recordings of excitatory post-synaptic potentials
    • reduced long term potentiation (MGI Ref ID J:109401)
      • CA1 hippocampal slices indicate brief post tetanic potentiation but no long term potentiation on recordings of excitatory post-synaptic potentials
  • abnormal nerve conduction (MGI Ref ID J:6323)
    • motor nerve conductance significantly lower than controls from 7 weeks of age onward
    • velocity returns to and is maintained at prediabetic levels by 15 weeks of age whereas control mice show a continuous increase in velocity
    • insulin treatment results in improved conductance but only for the duration of treatment and control levels of conductance are never restored
    • no conductance improvement is seen in mice over 23 weeks in age due to insulin treatment
  • abnormal nervous system morphology (MGI Ref ID J:6323)
    • abnormal axon morphology (MGI Ref ID J:6323)
      • non significant shift toward smaller fiber diameter at 15 weeks of age
      • significantly shifted to smaller diameter fibers by 25 weeks in ventral roots, dorsal roots, sural nerve
      • smaller diameter nerve fibers in peroneal, phrenic and vagus nerves at 25 weeks but not significant
      • small numbers of very large unmyelinated fibers (up to 1.6 micrometers)
      • shift of unmyelinated fibers to smaller diameters
      • abnormal myelin sheath morphology (MGI Ref ID J:6323)
        • number of myelin lamellae relative to nerve diameter is increased
    • abnormal axon outgrowth (MGI Ref ID J:112680)
      • axonal growth cone extension fails to occur for neurons treated in culture with 100ng/ml of leptin
    • decreased motor neuron number (MGI Ref ID J:6323)
      • myelinated fibers reduced in numbers at 25 weeks in the sural nerve
      • unmyelinated fibers reduced in numbers at 25 weeks in the vagus nerve
      • myelinated fiber density increases in most nerves (not the peroneal and phrenic nerves)
      • unmyelinated fiber density increase in the sural, peroneal, and vagus nerves
  • behavior/neurological phenotype
  • abnormal circadian rhythm (MGI Ref ID J:91813)
    • daily locomotor pattern becomes attenuated in 6-8 week old mice but rhythmicity is retained
    • daily locomotor activity rhythmicity severely diminished at 13-14 weeks, 75% fail to show significant rhythmicity
    • daily locomotor rhythmicity restored by feeding restriction during dark phase
  • abnormal food intake (MGI Ref ID J:43162)
    • food intake is about 60% of control level
  • abnormal learning/memory/conditioning (MGI Ref ID J:109401)
    • abnormal spatial learning (MGI Ref ID J:109401)
      • longer swimming distances than control mice in a Morris water maze test
    • abnormal spatial reference memory (MGI Ref ID J:109401)
      • cross the original platform location less frequently than do controls in a Morris water maze test
  • vision/eye phenotype
  • abnormal eye electrophysiology (MGI Ref ID J:103714)
    • prolonged latency of the b-wave in the retina
    • delays in oscillatory potentials 1, 2, 3 although only the delay in "OP1" is significant
  • digestive/alimentary phenotype
  • increased glucagon secretion (MGI Ref ID J:6264)
    • increased secreation of glucagon by pancreatic cells in culture
  • endocrine/exocrine gland phenotype
  • increased glucagon secretion (MGI Ref ID J:6264)
    • increased secreation of glucagon by pancreatic cells in culture
  • cardiovascular system phenotype
  • abnormal myocardial fiber morphology (MGI Ref ID J:6115)
    • presence of many lipid droplets
    • dense bodies present in places normally occupied by mitochondria
    • disrupted sarcomeres sometimes
  • abnormal vascular development (MGI Ref ID J:6115)
    • dense bodies found in the smooth muscle of intramyocardial arteries
  • muscle phenotype
  • abnormal myocardial fiber morphology (MGI Ref ID J:6115)
    • presence of many lipid droplets
    • dense bodies present in places normally occupied by mitochondria
    • disrupted sarcomeres sometimes

Leprdb/Leprdb

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

m/m

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

Gene & Allele Details

Allele Symbol Leprdb
Allele Name diabetes
Common Name(s) Lepdb; Lepr-; Leprdb-1J; db; leprdb;
Strain of OriginC57BLKS/J
Gene Symbol and Name Lepr, leptin receptor
Chromosome 4
Gene Common Name(s) CD295; Fa; LEPROT; Leprb; Modb1; 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]
 
Allele Symbol m
Allele Name misty
Strain of OriginDBA/J

Control Information

  Allele   Control
 Leprdb  m +/+ Leprdb or m +/m + from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Genotyping Protocols

Leprdb
m (Misty)

Colony Maintenance

Breeding & HusbandrySince both males and females homozygous for db 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, m +/+ 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 m and Leprdb loci is only about 2%. The homozygous misty phenotype is recognizable in pups as young as 3 days old by the absence of pigment in paws and tip of tail. The genotypes available to the customer are m+/m? (in which the ? is probably +), +Leprdb/?Leprdb (in which the ? is probably +), or ?+/+? (in which the ? are probably the mutant alleles). Dietary restrictions can prolong life and carbohydrate-free, protein-enriched defined diets can diminish significantly the severity of the disease. See the strain description (phenotype) for other husbandry related issues associated with this strain.
Diet Information LabDiet® 5K52/5K67

Related Strains

Strains carrying   Leprdb allele
002048   B6 x C57BLKS-m Leprdb Myo15sh2-J/J
000699   B6.Cg-m Leprdb/+ +/J
000642   BKS.Cg-m +/+ Leprdb/J
000700   BKS.Cg-m Leprdb/+ +/J
001192   BKS.Cg-meaJ Leprdb +/+ + m/J
000707   CBA.Cg-m Leprdb/+ +/J
006654   FVB.BKS(D)-Leprdb/ChuaJ
View Strains carrying   Leprdb     (7 strains)

View Strains carrying   m     (8 strains)

Strains carrying other alleles of Lepr
000709   129P3/J-Leprdb-3J/J
004939   NOD/ShiLtJ-Leprdb-5J/LtJ
006846   STOCK Leprdb-9J/Jgn
View Strains carrying other alleles of Lepr     (3 strains)

Phenotypic Data

Mouse Phenome Database

Additional Web Information

Congenic Nomenclature
Genetic Quality Control Annual Report

Animal Health Reports

Room Number           AX1

Research Applications

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

Diabetes and Obesity Research
Hyperglycemia (transient)
Type 2 Diabetes (NIDDM) (transient)

Internal/Organ Research
Wound Healing (delayed/impaired)

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 and Inflammation Research
Immunodeficiency Associated with Other Defects

Internal/Organ Research
Adipose Defects

Metabolism Research

Mouse/Human Gene Homologs
obesity, morbid, with hypogonadism (rare)

Reproductive Biology Research
Fertility Defects

m related

Dermatology Research
Color and White Spotting Defects

References

Selected Reference(s)

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. 1997. Mutant mice mimic human sickle cell anemia [news; comment] Science 278(5339):803-4. [PubMed: 9381190]  [MGI Ref ID J:44159]

Bates SH; Stearns WH; Dundon TA; Schubert M; Tso AW; Wang Y; Banks AS; Lavery HJ; Haq AK; Maratos-Flier E; Neel BG; Schwartz MW; Myers MG Jr. 2003. STAT3 signalling is required for leptin regulation of energy balance but not reproduction. Nature 421(6925):856-9. [PubMed: 12594516]  [MGI Ref ID J:82334]

Boillot D; Assan R; Dardenne M; Debray-Sachs M; Bach JF. 1986. T-lymphopenia and T-cell imbalance in diabetic db/db mice. Diabetes 35(2):198-203. [PubMed: 3510925]  [MGI Ref ID J:109948]

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]

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. 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]

Feliers D; Duraisamy S; Faulkner JL; Duch J; Lee AV; Abboud HE; Choudhury GG; Kasinath BS. 2001. Activation of renal signaling pathways in db/db mice with type 2 diabetes. Kidney Int 60(2):495-504. [PubMed: 11473632]  [MGI Ref ID J:109871]

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]

Giacomelli F; Wiener J. 1979. Primary myocardial disease in the diabetic mouse. An ultrastructural study. Lab Invest 40(4):460-73. [PubMed: 431046]  [MGI Ref ID J:6115]

Herberg L; Coleman DL. 1977. Laboratory animals exhibiting obesity and diabetes syndromes. Metabolism 26(1):59-99. [PubMed: 834144]  [MGI Ref ID J:5759]

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]

Johnson LM; Sidman RL. 1979. A reproductive endocrine profile in the diabetes (db) mutant mouse. Biol Reprod 20(3):552-9. [PubMed: 378276]  [MGI Ref ID J:6157]

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]

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; Coleman DL. 1989. The influence of genetic background on the expression of mutations at the diabetes locus in the mouse. V. Interaction between the db gene and hepatic sex steroid sulfotransferases correlates with gender-dependent susceptibility to hyperglycemia. Endocrinology 124(2):912-22. [PubMed: 2912706]  [MGI Ref ID J:26013]

Leiter EH; Coleman DL; Eppig JJ. 1979. Endocrine pancreatic cells of postnatal diabetes (db) mice in cell culture. In Vitro 15(7):507-21. [PubMed: 393618]  [MGI Ref ID J:6264]

Leiter EH; Coleman DL; Ingram DK; Reynolds MA. 1983. Influence of dietary carbohydrate on the induction of diabetes in C57BL/KsJ-db/db diabetes mice. J Nutr 113(1):184-95. [PubMed: 6337242]  [MGI Ref ID J:109957]

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]

MacLean PS; Bower JF; Vadlamudi S; Osborne JN; Bradfield JF; Burden HW; Bensch WH; Kauffman RF; Barakat HA. 2003. Cholesteryl ester transfer protein expression prevents diet-induced atherosclerotic lesions in male db/db mice. Arterioscler Thromb Vasc Biol 23(8):1412-5. [PubMed: 12791674]  [MGI Ref ID J:109846]

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]

Pasko KL; Salvin SB; Winkelstein A. 1981. Mechanisms in the in vivo release of lymphokines. V. Responses in alloxan-treated and genetically diabetic mice. Cell Immunol 62(1):205-19. [PubMed: 7261069]  [MGI Ref ID J:109959]

Sharma K; McCue P; Dunn SR. 2003. Diabetic kidney disease in the db/db mouse. Am J Physiol Renal Physiol 284(6):F1138-44. [PubMed: 12736165]  [MGI Ref ID J:83903]

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]

Sviderskaya EV; Novak EK; Swank RT; Bennett DC. 1998. The murine misty mutation: phenotypic effects on melanocytes, platelets and brown fat. Genetics 148(1):381-90. [PubMed: 9475748]  [MGI Ref ID J:45425]

Tian Z; Sun R; Wei H; Gao B. 2002. Impaired natural killer (NK) cell activity in leptin receptor deficient mice: leptin as a critical regulator in NK cell development and activation. Biochem Biophys Res Commun 298(3):297-302. [PubMed: 12413939]  [MGI Ref ID J:80037]

Tran KQ; Graewin SJ; Swartz-Basile DA; Nakeeb A; Svatek CL; Pitt HA. 2003. Leptin-resistant obese mice have paradoxically low biliary cholesterol saturation. Surgery 134(2):372-7. [PubMed: 12947343]  [MGI Ref ID J:109844]

Trayhurn P. 1979. Thermoregulation in the diabetic-obese (db/db) mouse. The role of non-shivering thermogenesis in energy balance. Pflugers Arch 380(3):227-32. [PubMed: 573463]  [MGI Ref ID J:6202]

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]

Yamashita H; Shao J; Ishizuka T; Klepcyk PJ; Muhlenkamp P; Qiao L; Hoggard N; Friedman JE. 2001. Leptin administration prevents spontaneous gestational diabetes in heterozygous Lepr(db/+) mice: effects on placental leptin and fetal growth. Endocrinology 142(7):2888-97. [PubMed: 11416008]  [MGI Ref ID J:71934]

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

Price and Supply Information

Strain Name: B6.Cg-m +/+ Leprdb/J
Stock Number: 000697

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Standard SupplyLevel 3. Up to 50 mice. Larger quantities or custom orders arranged upon request.
Supply Notes Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
Strains that must be genotyped are not available until five to seven weeks of age.
Genomic DNA is available for this strain from the Mouse DNA Resource.
LicensingSee General Terms and Conditions below  
Control InformationView Control Information in Strain Details.

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