Strain Name:

BKS.Cg-Lepob/J

Stock Number:

000696

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Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Former Names BKS.V-Lepob/J    (Changed: 18-JUL-12 )
Type Congenic; Mutant Strain;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain C57BLKS/J
Donor Strain V
H2 Haplotyped

Appearance
black, fat
Related Genotype: a/a Lepob/Lepob

black, lean
Related Genotype: a/a Lepob/+ or a/a ?/+

Description
Mice homozygous for the obese spontaneous mutation (Lepob, commonly referred to as ob or ob/ob) are first recognizable at about 4 weeks old. Homozygous mutant mice increase in weight rapidly and may reach three times the normal weight of wildtype controls. In addition to obesity, mutant mice exhibit hyperphagia; a diabetes-like syndrome of hyperglycemia, glucose intolerance, and elevated plasma insulin; subfertility; and increased hormone production from both pituitary and adrenal. They are also hypometabolic and hypothermic. The obesity is characterized by both an increased number and size of adipocytes. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase body weight and is probably the result of it. Homozygotes do have an abnormally low threshold for stimulation of pancreatic islet insulin secretion even in very young preobese animals. As is the case with the diabetes mutant (Lepdb), manifestation of the diabetic syndrome is strikingly dependent on genetic background. On the C57BLKS background Lepob/Lepobhomozygotes become severely diabetic with regression of islets and early death. Cloning of the Lep gene has made possible the production of recombinant leptin. Injection of this protein into Lepob/Lepob homozygotes sharply reduced body weight, decreased food intake, and increased energy expenditure.

Control Information

  Control
   Untyped from the colony
   000662 C57BLKS/J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Lepob allele
006906   B6.Cg-Lepob Ldlrtm1Her/J
000632   B6.Cg-Lepob/J
004824   BTBR.Cg-Lepob/WiscJ
View Strains carrying   Lepob     (3 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

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

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Lepob/Lepob

        BKS.Cg-Lepob/J
  • mortality/aging
  • premature death   (MGI Ref ID J:5400)
  • growth/size/body phenotype
  • increased growth rate
    • mice reach 45-55 g by 3-4 months of age   (MGI Ref ID J:5400)
    • slowly lose weight from 4 months on   (MGI Ref ID J:5400)
  • homeostasis/metabolism phenotype
  • abnormal circulating cholesterol level   (MGI Ref ID J:18161)
    • increased circulating cholesterol level
      • fasting plasma total cholesterol concentration is increased 2-3 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)
  • abnormal circulating glucose level   (MGI Ref ID J:5400)
    • hyperglycemia
      • blood sugar continues to rise   (MGI Ref ID J:5400)
      • blood sugar never returns to control levels   (MGI Ref ID J:5400)
      • stabilizes at around 400-500 mg/100 ml   (MGI Ref ID J:5400)
  • increased circulating insulin level
    • insulin levels increase only through the first 2 months   (MGI Ref ID J:5400)
    • levels drop back to normal   (MGI Ref ID J:5400)
  • increased circulating triglyceride level
    • triglyceride levels are elevated 1.5- to 2-fold   (MGI Ref ID J:18161)
  • increased urine glucose level   (MGI Ref ID J:5400)
  • endocrine/exocrine gland phenotype
  • abnormal pancreatic beta cell physiology
    • more beta cell degranulation than seen on the 'B6' background   (MGI Ref ID J:5400)
  • small pancreatic islets
    • after 2 months, islets become smaller and atrophic   (MGI Ref ID J:5400)
  • renal/urinary system phenotype
  • increased urine glucose level   (MGI Ref ID J:5400)
  • polyuria   (MGI Ref ID J:5400)

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

Lepob/Lep+

        involves: 129X1/SvJ * C57BL/6
  • liver/biliary system phenotype
  • increased liver weight
    • mice show significant increase in relative and absolute hepatic weight compared to wild-type; otherwise, no differences from wild-type are noted   (MGI Ref ID J:76479)

Lepob/Lep+

        involves: C57BL/6J
  • skeleton phenotype
  • increased bone mass
    • increased bone mass even on a low fat diet to delay obesity   (MGI Ref ID J:60001)

Lepob/Lepob

        Background Not Specified
  • growth/size/body phenotype
  • increased body weight   (MGI Ref ID J:159285)
  • homeostasis/metabolism phenotype
  • decreased liver triglyceride level
    • lower level than wild-type after 36 hour fasting in 7-week-old mice.   (MGI Ref ID J:199803)
  • increased liver triglyceride level
    • double the control littermate's triglyceride level in 7 to 14 weeks old mice   (MGI Ref ID J:199803)
  • liver/biliary system phenotype
  • decreased liver triglyceride level
    • lower level than wild-type after 36 hour fasting in 7-week-old mice.   (MGI Ref ID J:199803)
  • decreased susceptibility to hepatic steatosis
    • after 36 hour fasting in 7-week-old mice   (MGI Ref ID J:199803)
  • increased liver triglyceride level
    • double the control littermate's triglyceride level in 7 to 14 weeks old mice   (MGI Ref ID J:199803)

Lepob/Lepob

        involves: C57BL/6J
  • growth/size/body phenotype
  • abnormal postnatal growth
    • pair fed mice restrict food intake to that of controls   (MGI Ref ID J:6236)
    • pair fed mice gain less weight as protein than when feeding is unrestricted   (MGI Ref ID J:6236)
    • pair fed mice gain considerably more weight as fat than controls eating the same quantity of food   (MGI Ref ID J:6236)
    • pair fed mice gain less weight than when feeding is unrestricted   (MGI Ref ID J:6236)
  • obese   (MGI Ref ID J:92558)
  • endocrine/exocrine gland phenotype
  • abnormal insulin secretion
    • lower threshold for glucose induced insulin secretion by beta cells   (MGI Ref ID J:14402)
    • acetyl choline has a greater affect to lower the glucose induced threshold for insulin secretion   (MGI Ref ID J:22634)
  • homeostasis/metabolism phenotype
  • abnormal glucose homeostasis   (MGI Ref ID J:92558)
    • abnormal insulin secretion
      • lower threshold for glucose induced insulin secretion by beta cells   (MGI Ref ID J:14402)
      • acetyl choline has a greater affect to lower the glucose induced threshold for insulin secretion   (MGI Ref ID J:22634)
    • hyperglycemia   (MGI Ref ID J:92558)
    • impaired glucose tolerance
      • observed prior to any significant increase in body weight   (MGI Ref ID J:86303)
    • increased circulating insulin level   (MGI Ref ID J:92558)
  • abnormal hormone level   (MGI Ref ID J:13151)
    • abnormal corticosterone level
      • corticosterone response to stress greater than in controls   (MGI Ref ID J:13151)
      • diurnal variation greater than in controls   (MGI Ref ID J:13151)
      • increased circulating corticosterone level
    • increased adrenocorticotropin level
      • levels in the pituitary are much higher than in pituitaries of controls   (MGI Ref ID J:13151)
    • increased circulating insulin level   (MGI Ref ID J:92558)
  • 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 mass
    • denser vertebrae and long bones at 6 months   (MGI Ref ID J:60001)
    • increased bone mass even on a low fat diet to delay obesity   (MGI Ref ID J:60001)
    • osteopetrosis
      • increased numbers of thick trabeculae at 3 and 6 months   (MGI Ref ID J:60001)
      • 2 fold increase in trabecular bone volume   (MGI Ref ID J:60001)
  • hematopoietic system phenotype
  • abnormal osteoclast differentiation
    • increased numbers of osteoclasts   (MGI Ref ID J:60001)
  • adipose tissue phenotype
  • increased fat cell size   (MGI Ref ID J:5765)
  • digestive/alimentary phenotype
  • abnormal intestinal mucosa morphology
    • thick mucus gel covers the epithelium of the colon   (MGI Ref ID J:109110)
    • abnormal intestinal goblet cell morphology
      • increased number of mucus filled goblet cells in the colon   (MGI Ref ID J:109110)
  • cardiovascular system phenotype
  • abnormal cardiovascular system physiology
    • attenuated heart response to increased calcium   (MGI Ref ID J:116841)
    • oxygen consumption of the heart does not increase with an increased workload   (MGI Ref ID J:116841)
    • oxygen consumption is elevated when perfused with glucose and palmitate   (MGI Ref ID J:116841)
  • abnormal retinal vasculature morphology
    • neovascularization is significantly suppressed under standard oxygen conditions relative to controls   (MGI Ref ID J:92072)
  • increased heart weight
    • heart weight elevated relative to controls   (MGI Ref ID J:116841)
  • muscle phenotype
  • abnormal muscle contractility
    • basal calcium ion concentration increases sharply toward the end of a series of 50 tetanic contractions (single cell measures)   (MGI Ref ID J:106205)
    • number of tetani required to reduce force by 40% is significantly less than for controls   (MGI Ref ID J:106205)
  • vision/eye phenotype
  • abnormal retinal vasculature morphology
    • neovascularization is significantly suppressed under standard oxygen conditions relative to controls   (MGI Ref ID J:92072)
  • nervous system phenotype
  • decreased nerve conduction velocity
    • 16% lower motor nerve conduction velocity than controls   (MGI Ref ID J:121015)
    • hind limb sensory nerve conduction velocity reduced 22%   (MGI Ref ID J:121015)
  • behavior/neurological phenotype
  • abnormal behavior
    • faster in food finding trials relative to controls   (MGI Ref ID J:112820)
    • increased thermal nociceptive threshold
      • 88% increased latency of hind-limb withdrawal from a heat stimulus   (MGI Ref ID J:121015)
  • 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)
  • abnormal respiratory electron transport chain
    • mitochondrial respiration is inhibited in glucose perfused hearts   (MGI Ref ID J:116841)
    • increased ADP dependent mitochondrial respiration in glucose and palmitate perfused hearts   (MGI Ref ID J:116841)
    • mitochondrial respiration is uncoupled in glucose and palmitate perfused hearts   (MGI Ref ID J:116841)
  • integument phenotype
  • abnormal epidermal layer morphology
    • significant reduction in intraepidermal nerve fiber density   (MGI Ref ID J:121015)
  • increased thermal nociceptive threshold
    • 88% increased latency of hind-limb withdrawal from a heat stimulus   (MGI Ref ID J:121015)

Lepob/Lepob

        B6.Cg-Lepob/J
  • growth/size/body phenotype
  • abnormal body weight
    • treatment with triiodothyronine significantly reduces body weight relative to the reduction seen in controls   (MGI Ref ID J:22025)
    • body weight reduced by treatment with Leptin   (MGI Ref ID J:29075)
    • increased body weight   (MGI Ref ID J:185261)
      • obese
        • 12-week old males are obese   (MGI Ref ID J:104171)
        • develop progressive obesity   (MGI Ref ID J:103063)
  • increased growth rate
    • mice reach 60-70 g by 10 months of age   (MGI Ref ID J:5400)
  • increased percent body fat
    • mice have fat mass of ~42 g compared to ~3 g in wild-type at 16 weeks   (MGI Ref ID J:122746)
  • homeostasis/metabolism phenotype
  • abnormal circulating cholesterol level   (MGI Ref ID J:18161)
    • increased circulating cholesterol level
      • fasting plasma total cholesterol concentration is increased 2-3 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)
  • abnormal circulating glucose level   (MGI Ref ID J:5400)
    • decreased circulating glucose level
      • after feeding, serum glucose levels are more than 30% lower than in wild-type mice   (MGI Ref ID J:145998)
      • hypoglycemia
        • older mice are usually hypoglycemic   (MGI Ref ID J:5400)
    • hyperglycemia
      • serum glucose is 320 mg/dl compared to 134 mg/dl in wild-type controls   (MGI Ref ID J:122746)
      • transient hyperglycemia   (MGI Ref ID J:5400)
      • blood sugar peaks at 2-3 months   (MGI Ref ID J:5400)
      • returns to normal by 4-5 months of age   (MGI Ref ID J:5400)
      • homozygotes exhibit a mild, transient hyperglycemia between 10-14 weeks of age as compared to the severe, progressive hyperglycemia observed on the BTBR background   (MGI Ref ID J:65486)
      • mice infrequently transition to severe hyperglycemia   (MGI Ref ID J:65486)
      • males exhibit elevated blood glucose levels (254.4 +/-33.7 mg/dl) as compared to wild-type between 20-22 weeks of age   (MGI Ref ID J:185261)
      • blood glucose levels are lower than obese mice on the BTBR background   (MGI Ref ID J:185261)
  • abnormal oxygen consumption
    • oxygen consumption about 2/3 that observed in controls   (MGI Ref ID J:22025)
    • increased by treatment with triiodothyronine   (MGI Ref ID J:22025)
    • insulin stimulated oxygen consumption by the soleus muscle is little affected by triiodothyronine   (MGI Ref ID J:22377)
    • decreased oxygen consumption
      • in the epididymal and brown fat pads   (MGI Ref ID J:22377)
    • increased oxygen consumption
      • in the liver   (MGI Ref ID J:22377)
  • abnormal protein level
    • total body protein lower than in controls   (MGI Ref ID J:22025)
    • total body protein increased by treatment with triiodothyronine   (MGI Ref ID J:22025)
  • abnormal urine homeostasis
    • males show elevated levels of serotonin and 5'hydroxyindolineacetic acid in urine   (MGI Ref ID J:4033)
    • abnormal urine catecholamine level
      • less epinephrine in the urine of ad libitum fed mice   (MGI Ref ID J:4033)
      • urine levels of norepinephrine only slightly elevated   (MGI Ref ID J:4033)
      • males show elevated levels of dopamine in urine   (MGI Ref ID J:4033)
  • decreased body temperature
    • body temperature is maintained a basal level when the ambient temperature is gradually reduced to 4C   (MGI Ref ID J:129662)
  • decreased insulin secretion
    • leptin-treated islet cells exhibit decreased insulin secretion compared to similarly treated wild-type islets   (MGI Ref ID J:145998)
  • impaired glucose tolerance   (MGI Ref ID J:104171)
    • glucose intolerance which improved when treated with rosiglitazone   (MGI Ref ID J:107486)
    • following an acute intraperitoneal glucose injection, the post-challenge glucose level remained elevated up to 120 min compared to controls, indicating glucose intolerance   (MGI Ref ID J:107486)
  • increased circulating insulin level
    • seen in 12-week old males   (MGI Ref ID J:104171)
    • serum insulin is 41.5 ng/ml compared to 0.8 ng/ml in wild-type   (MGI Ref ID J:122746)
    • at 2 weeks, insulin levels are increased 2.5-fold compared to in wild-type mice   (MGI Ref ID J:145998)
    • however, mice treated with isoproterenol exhibit lowered serum levels of insulin   (MGI Ref ID J:145998)
    • insulin levels increase rapidly to over 50X normal controls   (MGI Ref ID J:5400)
  • increased circulating triglyceride level
    • seen in 12-week old males   (MGI Ref ID J:104171)
    • triglyceride levels are elevated 1.5- to 2-fold   (MGI Ref ID J:18161)
  • increased insulin secretion
    • insulin content in the pancreata is increased compared to in wild-type mice   (MGI Ref ID J:145998)
  • insulin resistance   (MGI Ref ID J:104171)
  • cardiovascular system phenotype
  • abnormal myocardial fiber morphology
    • exhibit extensive focal damage in myocardial tissue, showing an abundance of lipid droplets in myocytes and damaged mitochondria that are swelled, have disorganized cristae and show loss of integrity   (MGI Ref ID J:104171)
    • exhibit myocyte hypertrophy, with increased myocyte diameter and distorted nuclear architecture   (MGI Ref ID J:103063)
    • cardiomyocytes exhibit a significantly enlarged cross-sectional area   (MGI Ref ID J:111488)
    • enlarged myocardial fiber
      • cardiomyocytes display larger resting cell length and cross-sectional area   (MGI Ref ID J:104171)
  • abnormal myocardial fiber physiology
    • cardiomyocytes exhibit decreased peak shortening and maximal velocity of shortening/relengthening, prolonged time-to-90% relengthening, reduced intracellular calcium release upon electrical stimulus associated with a slowed intracellular calcium decay rate, and significantly higher oxygen levels   (MGI Ref ID J:104171)
  • decreased cardiac muscle contractility
    • exhibit cardiac contractile dysfunction that is due to leptin deficiency and not obesity as high fat diet-induced obese controls show normal cardiomyocyte morphology and contractile function   (MGI Ref ID J:104171)
    • cardiomyocytes exhibit a reduced contractile capacity   (MGI Ref ID J:111488)
    • decreased peak shortening   (MGI Ref ID J:111488)
    • prolonged relengthening   (MGI Ref ID J:111488)
    • elevated resting peak calcium ion concentration   (MGI Ref ID J:111488)
    • slowed intracellular calcium ion decay   (MGI Ref ID J:111488)
  • 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 muscle morphology
    • muscle protein content is reduced   (MGI Ref ID J:151518)
    • abnormal myocardial fiber morphology
      • exhibit extensive focal damage in myocardial tissue, showing an abundance of lipid droplets in myocytes and damaged mitochondria that are swelled, have disorganized cristae and show loss of integrity   (MGI Ref ID J:104171)
      • exhibit myocyte hypertrophy, with increased myocyte diameter and distorted nuclear architecture   (MGI Ref ID J:103063)
      • cardiomyocytes exhibit a significantly enlarged cross-sectional area   (MGI Ref ID J:111488)
      • enlarged myocardial fiber
        • cardiomyocytes display larger resting cell length and cross-sectional area   (MGI Ref ID J:104171)
    • abnormal skeletal muscle fiber type ratio
      • lower proportion of faster myosin heavy chain isoforms   (MGI Ref ID J:151518)
    • decreased skeletal muscle fiber size
      • cross-sectional area of muscle fibers is generally smaller   (MGI Ref ID J:151518)
    • decreased skeletal muscle mass
      • mean muscle mass consistently less than controls but magnitude of difference is muscle specific   (MGI Ref ID J:151518)
  • decreased cardiac muscle contractility
    • exhibit cardiac contractile dysfunction that is due to leptin deficiency and not obesity as high fat diet-induced obese controls show normal cardiomyocyte morphology and contractile function   (MGI Ref ID J:104171)
    • cardiomyocytes exhibit a reduced contractile capacity   (MGI Ref ID J:111488)
    • decreased peak shortening   (MGI Ref ID J:111488)
    • prolonged relengthening   (MGI Ref ID J:111488)
    • elevated resting peak calcium ion concentration   (MGI Ref ID J:111488)
    • slowed intracellular calcium ion decay   (MGI Ref ID J:111488)
  • adipose tissue phenotype
  • abnormal adipose tissue amount
    • treatment with triiodothyronine significantly reduces adipocyte numbers relative to the degree of reduction seen in controls   (MGI Ref ID J:22377)
    • treatment with triiodothyronine reduces adipocyte numbers   (MGI Ref ID J:22377)
    • increased percent body fat
      • mice have fat mass of ~42 g compared to ~3 g in wild-type at 16 weeks   (MGI Ref ID J:122746)
  • abnormal epididymal fat pad morphology
    • treatment with triiodothyronine significantly reduces epididymal fat pad weight relative to the degree of reduction seen in controls   (MGI Ref ID J:22377)
    • adipocyte size remains larger after treatment with triiodothyronine relative to controls   (MGI Ref ID J:22377)
  • increased fat cell size   (MGI Ref ID J:189019)
  • increased interscapular fat pad weight
    • greater weight than for controls   (MGI Ref ID J:22377)
    • affected less by treatment with triiodothyronine than controls   (MGI Ref ID J:22377)
    • brown adipocyte numbers are normal   (MGI Ref ID J:22377)
  • behavior/neurological phenotype
  • abnormal food intake   (MGI Ref ID J:122746)
    • decreased food intake
      • food intake is reduced by Leptin treatment   (MGI Ref ID J:29075)
    • increased food intake
      • increased food intake when ambient temperature drops from 28 to 21C   (MGI Ref ID J:129662)
      • polyphagia
        • mice eat 70% more than wild-type controls   (MGI Ref ID J:122746)
  • abnormal pain threshold   (MGI Ref ID J:152019)
    • allodynia
      • resistant to tactile allodynia caused by partial sciatic nerve ligation   (MGI Ref ID J:152019)
      • epineural application of leptin treated peritoneal macrophage induces tactile allodynia   (MGI Ref ID J:152019)
    • hyperalgesia
      • display thermal hyperalgesia after partial sciatic nerve ligation   (MGI Ref ID J:152019)
  • abnormal sleep pattern
    • increased total sleep time in a 24 hour period   (MGI Ref ID J:115771)
    • additional sleep primarily in the dark phase   (MGI Ref ID J:115771)
    • increased non-REM sleep time   (MGI Ref ID J:115771)
    • recovery from sleep deprivation involves increased duration of non-REM bouts rather than increased number of bouts as seen in controls   (MGI Ref ID J:115771)
    • abnormal frequency of paradoxical sleep
      • reduced REM in light phase   (MGI Ref ID J:115771)
      • increased REM in dark phase   (MGI Ref ID J:115771)
    • fragmentation of sleep/wake states
      • sleep more fragmented   (MGI Ref ID J:115771)
      • more arousals   (MGI Ref ID J:115771)
      • shorter wake periods   (MGI Ref ID J:115771)
  • hypoactivity
    • significantly reduced activity relative to wild-type controls   (MGI Ref ID J:122746)
    • less wheel running activity   (MGI Ref ID J:115771)
    • more wheel running activity in light phase and less in dark phase   (MGI Ref ID J:115771)
  • reproductive system phenotype
  • female infertility
    • females do not produce litters   (MGI Ref ID J:122746)
  • respiratory system phenotype
  • lung inflammation
    • 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)
  • endocrine/exocrine gland phenotype
  • abnormal pancreatic beta cell physiology
    • less beta cell degranulation than seen on the "BKS" background   (MGI Ref ID J:5400)
    • decreased insulin secretion
      • leptin-treated islet cells exhibit decreased insulin secretion compared to similarly treated wild-type islets   (MGI Ref ID J:145998)
    • increased insulin secretion
      • insulin content in the pancreata is increased compared to in wild-type mice   (MGI Ref ID J:145998)
  • enlarged pancreatic islets   (MGI Ref ID J:5400)
  • renal/urinary system phenotype
  • abnormal urine homeostasis
    • males show elevated levels of serotonin and 5'hydroxyindolineacetic acid in urine   (MGI Ref ID J:4033)
    • abnormal urine catecholamine level
      • less epinephrine in the urine of ad libitum fed mice   (MGI Ref ID J:4033)
      • urine levels of norepinephrine only slightly elevated   (MGI Ref ID J:4033)
      • males show elevated levels of dopamine in urine   (MGI Ref ID J:4033)
  • immune system phenotype
  • decreased NK cell number
    • reduced numbers can be restored by treatment with leptin   (MGI Ref ID J:117826)
  • lung inflammation
    • 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)
  • 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)
    • leptin reduces the level of metastasis   (MGI Ref ID J:117826)
  • hematopoietic system phenotype
  • decreased NK cell number
    • reduced numbers can be restored by treatment with leptin   (MGI Ref ID J:117826)
  • nervous system phenotype
  • abnormal sympathetic nervous system physiology   (MGI Ref ID J:145998)
  • liver/biliary system phenotype
  • abnormal liver weight
    • treatment with triiodothyronine significantly reduces relative and absolute liver weight   (MGI Ref ID J:22377)
  • integument phenotype
  • abnormal pain threshold   (MGI Ref ID J:152019)
    • allodynia
      • resistant to tactile allodynia caused by partial sciatic nerve ligation   (MGI Ref ID J:152019)
      • epineural application of leptin treated peritoneal macrophage induces tactile allodynia   (MGI Ref ID J:152019)
    • hyperalgesia
      • display thermal hyperalgesia after partial sciatic nerve ligation   (MGI Ref ID J:152019)
  • skeleton phenotype
  • abnormal bone marrow morphology
    • bone marrow is almost completely replaced with mature adipocytes   (MGI Ref ID J:189019)

Lepob/Lepob

        D2.B6-Lepob
  • growth/size/body phenotype
  • obese   (MGI Ref ID J:78850)
  • homeostasis/metabolism phenotype
  • hyperglycemia
    • at 3 months of age, males are hyperglycemic with blood glucose levels of ~574 mg/dl; females have levels of ~388 mg/dl   (MGI Ref ID J:78850)
  • increased circulating insulin level
    • some mutant DBA/2J mice have high insulin levels compared to controls   (MGI Ref ID J:78850)
  • endocrine/exocrine gland phenotype
  • abnormal pancreatic islet morphology
    • islets of mutants with low insulin levels are abnormal in appearance, being found in clusters of 1-4 cells, scattered within the ductal epithelium   (MGI Ref ID J:78850)
    • decreased pancreatic beta cell number
      • mutants with low insulin secretion have a low number of insulin-secreting cells compared to controls or high-insulin secreting mutants   (MGI Ref ID J:78850)
    • increased pancreatic beta cell number
      • there is a 5-fold increase in number of insulin-secreting cells per islet in obese mice with high insulin secretion   (MGI Ref ID J:78850)

Lepob/Lepob

        FVB.B6-Lepob
  • homeostasis/metabolism phenotype
  • hyperglycemia
    • mice are hyperglycemic like congenic FVB Lepr mice   (MGI Ref ID J:78850)
  • increased circulating insulin level
    • mice are hyperinsulinemic like congenic FVB Leprdb mice   (MGI Ref ID J:78850)

Lepob/Lepob

        involves: 129X1/SvJ * C57BL/6
  • growth/size/body phenotype
  • decreased lean body mass
    • decreased (16.0 g, 33% of body weight) compared to wild-type (25.5 g 87% of body weight) or double mutants (19.8g)   (MGI Ref ID J:107169)
  • increased body weight
    • higher than wild-type   (MGI Ref ID J:107169)
  • homeostasis/metabolism phenotype
  • abnormal circulating hormone level   (MGI Ref ID J:76479)
    • abnormal circulating pancreatic peptide level
      • plasma levels of pancreatic polypeptide (PP) are strongly reduced compared to wild-type   (MGI Ref ID J:76479)
    • decreased circulating testosterone level
      • level is markedly decreased compared to wild-type or Lep heterozygotes   (MGI Ref ID J:76479)
      • significantly lower (4.2 nmol/l) compared to wild-type (14.2 nmol/l)   (MGI Ref ID J:107169)
    • increased circulating corticosterone level
      • mice display hypercorticosteronemia compared to wild-type   (MGI Ref ID J:76479)
      • mice display hypercorticosteronemia compared to wild-type, Npy2rtm1.1Hhz homozygotes, or Npy2r, Lep double mutants   (MGI Ref ID J:107169)
    • increased circulating insulin level
      • level is significantly increased over wild-type   (MGI Ref ID J:76479)
      • hyperinsulinemic compared to wild-type   (MGI Ref ID J:107169)
    • increased circulating leptin level
      • level is significantly increased over wild-type   (MGI Ref ID J:76479)
  • hyperglycemia   (MGI Ref ID J:107169)
  • increased circulating cholesterol level
    • 5.74 mmol/l vs 3.54 mmol/l in wild-type   (MGI Ref ID J:107169)
  • increased circulating triglyceride level
    • 2.48 mmol/l vs 1.62 mmol/l in wild-type   (MGI Ref ID J:107169)
  • endocrine/exocrine gland phenotype
  • abnormal branching of the mammary ductal tree
    • in virgin females, no ductal development occurs   (MGI Ref ID J:76479)
  • abnormal ovarian folliculogenesis
    • ovaries have very few primary or secondary follicles   (MGI Ref ID J:76479)
  • absent corpus luteum
    • no corpora lutea develops properly in ovary   (MGI Ref ID J:76479)
  • decreased seminal vesicle weight
    • weight of gland is significantly lower than wild-type or heterozygotes   (MGI Ref ID J:76479)
  • decreased testis weight
    • testis weight is significantly lower than in Lepob heterozygotes or Lep, Ppyr1 double null mice   (MGI Ref ID J:76479)
    • testes weigh 0.19 g compared to 0.33 g in wild-type   (MGI Ref ID J:107169)
  • increased pancreas weight
    • 0.41 g vs 0.29 in wild-type   (MGI Ref ID J:107169)
  • adipose tissue phenotype
  • abnormal adipose tissue amount
    • combined white adipose tissue (WAT) mass is increased compared to wild-type   (MGI Ref ID J:107169)
  • reproductive system phenotype
  • abnormal ovarian folliculogenesis
    • ovaries have very few primary or secondary follicles   (MGI Ref ID J:76479)
  • abnormal vagina orifice morphology
    • vaginal opening is very small compared to wild-type   (MGI Ref ID J:76479)
  • absent corpus luteum
    • no corpora lutea develops properly in ovary   (MGI Ref ID J:76479)
  • decreased seminal vesicle weight
    • weight of gland is significantly lower than wild-type or heterozygotes   (MGI Ref ID J:76479)
  • decreased testis weight
    • testis weight is significantly lower than in Lepob heterozygotes or Lep, Ppyr1 double null mice   (MGI Ref ID J:76479)
    • testes weigh 0.19 g compared to 0.33 g in wild-type   (MGI Ref ID J:107169)
  • female infertility
    • homozygous females produce no litters   (MGI Ref ID J:76479)
  • male infertility
    • only one male tested was able to sire a litter   (MGI Ref ID J:76479)
    • no males could produce offspring   (MGI Ref ID J:107169)
  • prolonged diestrus
    • mice have diestrous-like swab until 9 weeks of age   (MGI Ref ID J:76479)
  • prolonged estrous cycle
    • beginning at 9 weeks of age, estrous cycles last 11-15 days   (MGI Ref ID J:76479)
  • prolonged estrus
    • beginning at 9 weeks of age, estrous-like cytology lasts 6-8 days   (MGI Ref ID J:76479)
  • behavior/neurological phenotype
  • polyphagia   (MGI Ref ID J:107169)
  • digestive/alimentary phenotype
  • abnormal intestine morphology
    • mice display intestinal hypertrophy compared to wild-type mice (intestine weight - 1.89 g vs 1.03 g in wild-type; intestine length 43 cm vs 33 cm in wild-type)   (MGI Ref ID J:107169)
  • liver/biliary system phenotype
  • increased liver weight
    • 4.56 g vs 1.44 g in wild-type   (MGI Ref ID J:107169)
  • renal/urinary system phenotype
  • increased kidney weight
    • 0.54 g vs 0.41 g in wild-type   (MGI Ref ID J:107169)
  • integument phenotype
  • abnormal branching of the mammary ductal tree
    • in virgin females, no ductal development occurs   (MGI Ref ID J:76479)

Lepob/Lepob

        involves: 129/Sv * C57BL/6
  • homeostasis/metabolism phenotype
  • abnormal lipid level
    • sphingomeylin and antioxidant ethanolamine plasmlogen are markedly decreased   (MGI Ref ID J:121534)
  • increased circulating insulin level
    • at 4 and 16 weeks of age   (MGI Ref ID J:121534)
  • increased insulin secretion
    • at 16 weeks of age   (MGI Ref ID J:121534)
  • insulin resistance
  • endocrine/exocrine gland phenotype
  • abnormal pancreatic islet morphology
    • at 16 weeks, increased islet-to-pancreases volume ratios   (MGI Ref ID J:121534)
    • at 16 weeks, islet insulin content is 30-fold greater than in Ppargtm1Avb Lepob homozygotes   (MGI Ref ID J:121534)
    • enlarged pancreatic islets   (MGI Ref ID J:121534)
    • increased pancreatic islet number   (MGI Ref ID J:121534)
  • increased insulin secretion
    • at 16 weeks of age   (MGI Ref ID J:121534)
  • behavior/neurological phenotype
  • hypoactivity
    • at 20 weeks, mice have decreased locomotor activity compared to wild-type   (MGI Ref ID J:121534)
  • polyphagia
  • growth/size/body phenotype
  • increased body weight
    • mice quickly become heavier and have significantly elevated body weights at 4 and 6 weeks of age in females and males, respectively   (MGI Ref ID J:121534)
  • increased percent body fat
    • 40% increase compared to wild-type at 20 weeks   (MGI Ref ID J:121534)
  • adipose tissue phenotype
  • increased percent body fat
    • 40% increase compared to wild-type at 20 weeks   (MGI Ref ID J:121534)
  • liver/biliary system phenotype
  • hepatic steatosis   (MGI Ref ID J:121534)

Lepob/Lepob

        C57BL/6J-Lepob
  • homeostasis/metabolism phenotype
  • decreased circulating glucose level
    • when treated with AdipoR2-ASO, mice exhibit a decrease in plasma glucose level   (MGI Ref ID J:129554)

Lepob/Lepob

        B6.Cg-Lepob/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)

Lepob/Lepob

        B6.Cg-Lepob/JBomTac
  • homeostasis/metabolism phenotype
  • increased circulating triglyceride level

Lepob/Lepob

        involves: V
  • growth/size/body phenotype
  • decreased body length
    • first noticeable at 4-6 weeks of age   (MGI Ref ID J:13066)
    • short body   (MGI Ref ID J:13066)
    • square shape   (MGI Ref ID J:13066)
    • expansive hind quarters   (MGI Ref ID J:13066)
  • increased growth rate
    • begin to gain weight rapidly by 4-6 weeks of age   (MGI Ref ID J:13066)
    • weigh twice as much as controls at 3 months of age   (MGI Ref ID J:13066)
    • weigh 75-90g at 10 months   (MGI Ref ID J:13066)
  • behavior/neurological phenotype
  • polyphagia
    • hyperphagia   (MGI Ref ID J:7702)
  • homeostasis/metabolism phenotype
  • abnormal glucose homeostasis   (MGI Ref ID J:7702)
    • hyperglycemia
      • transient hyperglycemia   (MGI Ref ID J:7702)
    • impaired glucose tolerance   (MGI Ref ID J:7702)
    • increased circulating insulin level   (MGI Ref ID J:7702)
  • abnormal hormone level
    • increased beta endorphin levels   (MGI Ref ID J:7702)
    • increased levels of melanocyte stimulating hormone   (MGI Ref ID J:7702)
    • increased adrenocorticotropin level
      • increased pituitary ACTH   (MGI Ref ID J:7702)
    • increased circulating insulin level   (MGI Ref ID J:7702)
  • abnormal vascular wound healing
    • reduced neointimal area relative to controls 4 weeks after femoral artery injury   (MGI Ref ID J:135034)
    • neointimal area increased by leptin injection or adenoviral leptin treatment   (MGI Ref ID J:135034)
    • vascular smooth muscle proliferation significantly reduced   (MGI Ref ID J:135034)
  • decreased body temperature
    • mice have a lower basal body temperature than controls   (MGI Ref ID J:12010)
  • decreased circulating tumor necrosis factor level
    • 48% of control levels after kainate injection   (MGI Ref ID J:115569)
  • impaired adaptive thermogenesis
    • extreme cold susceptibility   (MGI Ref ID J:7702)
    • mice moved directly to 4C from 21C become hypothermic and die   (MGI Ref ID J:7702)
    • mice acclimated to 12C before exposure survive better to 4C exposure than un-acclimated controls   (MGI Ref ID J:7702)
    • 60 minute exposure of 17 day old mice to 4C results in a marked drop in body temperature   (MGI Ref ID J:12010)
  • endocrine/exocrine gland phenotype
  • abnormal gland physiology   (MGI Ref ID J:7702)
    • decreased activity of thyroid   (MGI Ref ID J:7702)
    • hypersecretion of corticosterone
      • increased glucocorticoids from the adrenal   (MGI Ref ID J:7702)
  • abnormal pancreatic beta cell morphology   (MGI Ref ID J:7702)
    • increased pancreatic beta cell mass
      • increased size   (MGI Ref ID J:7702)
    • increased pancreatic beta cell number   (MGI Ref ID J:7702)
  • adipose tissue phenotype
  • abnormal fat cell morphology   (MGI Ref ID J:5253)
    • hyperplasia   (MGI Ref ID J:7702)
    • increased fat cell size   (MGI Ref ID J:7702)
  • skeleton phenotype
  • abnormal long bone epiphyseal plate morphology
    • more fragile than controls   (MGI Ref ID J:102535)
    • failure at a force of 4.9 Newtons as compared to 8.4 Newtons in controls   (MGI Ref ID J:102535)
    • breakage at the chondro-osseous junction   (MGI Ref ID J:102535)
    • reduced expression of "type-X" collagen   (MGI Ref ID J:102535)
    • less organized loose reticular distribution of collagen fibrils   (MGI Ref ID J:102535)
    • abnormal long bone epiphyseal plate proliferative zone
      • column structure is disturbed   (MGI Ref ID J:102535)
      • poor alignment   (MGI Ref ID J:102535)
    • abnormal long bone hypertrophic chondrocyte zone
      • column structure is disturbed   (MGI Ref ID J:102535)
      • poor alignment   (MGI Ref ID J:102535)
      • mostly mineralized as compared to less than 50% mineralized in controls   (MGI Ref ID J:102535)
      • increased numbers of apoptotic chondrocytes   (MGI Ref ID J:102535)
  • decreased bone mass
    • reduced bone mass   (MGI Ref ID J:7702)
  • decreased length of long bones   (MGI Ref ID J:102535)
  • reproductive system phenotype
  • infertility   (MGI Ref ID J:7702)
    • female infertility
      • homozygous females fail to ovulate   (MGI Ref ID J:7702)
    • male infertility
      • all older males are sterile   (MGI Ref ID J:7702)
  • reduced male fertility
    • only 20% of young males are fertile   (MGI Ref ID J:7702)
  • nervous system phenotype
  • abnormal cortical plate morphology
    • fewer cells in the cortical plate at E18   (MGI Ref ID J:105139)
  • abnormal embryonic neuroepithelium morphology
    • significantly fewer cells at E16 and E18 but not at E14   (MGI Ref ID J:105139)
    • cell proliferation is lower at E14 and E16   (MGI Ref ID J:105139)
    • decreased embryonic neuroepithelium thickness
  • abnormal microglial cell physiology
    • 30-40% as many activated microglia 5 days after kainic acid treatment as for controls   (MGI Ref ID J:115569)
    • migrate normally to injury sites but do not proliferate   (MGI Ref ID J:115569)
  • decreased embryonic neuroepithelial cell proliferation
    • cell proliferation is lower at E14 and E16   (MGI Ref ID J:105139)
  • cardiovascular system phenotype
  • abnormal arteriole morphology
    • basal arteriolar diameter is greater than controls   (MGI Ref ID J:151096)
    • potassium-ATP channel inhibition eliminates diameter difference from controls   (MGI Ref ID J:151096)
  • abnormal vascular wound healing
    • reduced neointimal area relative to controls 4 weeks after femoral artery injury   (MGI Ref ID J:135034)
    • neointimal area increased by leptin injection or adenoviral leptin treatment   (MGI Ref ID J:135034)
    • vascular smooth muscle proliferation significantly reduced   (MGI Ref ID J:135034)
  • immune system phenotype
  • abnormal microglial cell physiology
    • 30-40% as many activated microglia 5 days after kainic acid treatment as for controls   (MGI Ref ID J:115569)
    • migrate normally to injury sites but do not proliferate   (MGI Ref ID J:115569)
  • decreased circulating tumor necrosis factor level
    • 48% of control levels after kainate injection   (MGI Ref ID J:115569)
  • limbs/digits/tail phenotype
  • short femur   (MGI Ref ID J:102535)
  • short humerus   (MGI Ref ID J:102535)
  • embryogenesis phenotype
  • abnormal embryonic neuroepithelium morphology
    • significantly fewer cells at E16 and E18 but not at E14   (MGI Ref ID J:105139)
    • cell proliferation is lower at E14 and E16   (MGI Ref ID J:105139)
    • decreased embryonic neuroepithelium thickness
  • hematopoietic system phenotype
  • abnormal microglial cell physiology
    • 30-40% as many activated microglia 5 days after kainic acid treatment as for controls   (MGI Ref ID J:115569)
    • migrate normally to injury sites but do not proliferate   (MGI Ref ID J:115569)

Lepob/Lepob

        involves: C57BL/6
  • homeostasis/metabolism phenotype
  • increased circulating cholesterol level
    • seen at 3-4 months of age   (MGI Ref ID J:72027)
    • increased circulating HDL cholesterol level
      • slightly elevated at 3 and 8 months of age   (MGI Ref ID J:72027)
  • increased circulating triglyceride level
    • seen at 3-4 months of age   (MGI Ref ID J:72027)
  • increased liver cholesterol level
    • livers exhibit slightly, but significantly, higher levels of cholesterol   (MGI Ref ID J:72027)
  • increased liver triglyceride level
    • livers exhibit about 10x higher levels of triglyceride   (MGI Ref ID J:72027)
  • liver/biliary system phenotype
  • increased liver cholesterol level
    • livers exhibit slightly, but significantly, higher levels of cholesterol   (MGI Ref ID J:72027)
  • increased liver triglyceride level
    • livers exhibit about 10x higher levels of triglyceride   (MGI Ref ID J:72027)
  • immune system phenotype
  • decreased CD4-positive T cell number   (MGI Ref ID J:164339)
  • decreased T cell proliferation   (MGI Ref ID J:164339)
  • decreased splenocyte number   (MGI Ref ID J:164339)
  • hematopoietic system phenotype
  • decreased CD4-positive T cell number   (MGI Ref ID J:164339)
  • decreased T cell proliferation   (MGI Ref ID J:164339)
  • decreased splenocyte number   (MGI Ref ID J:164339)

Lepob/Lepob

        BTBR.B6(Cg)-Lepob
  • homeostasis/metabolism phenotype
  • hyperglycemia
    • homozygotes exhibit severe, progressive hyperglycemia between 10-14 weeks of age as compared to the mild, transient hyperglycemia observed on the C57BL/6 background   (MGI Ref ID J:65486)

Lepob/Lepob

        (B6.Cg-Lepob/J x BTBR.B6(Cg)-Lepob)F2
  • endocrine/exocrine gland phenotype
  • decreased pancreatic beta cell number
    • severely diabetic mice exhibit reduced numbers of beta cells   (MGI Ref ID J:65486)
  • disorganized pancreatic islets
    • moderate to severely diabetic F2 mice have no hyperplasia, but exhibit cellular disorganization and fibrosis   (MGI Ref ID J:65486)
    • severely diabetic F2 mice exhibit concavities with acinar tissue intrusions   (MGI Ref ID J:65486)
  • pancreatic islet hyperplasia
    • mildly diabetic F2 mice exhibit large numbers of hyperplastic pancreatic islets   (MGI Ref ID J:65486)
  • homeostasis/metabolism phenotype
  • hyperglycemia
    • homozygotes exhibit a 7.5 fold range in fasting glucose (100-750 mg/dl)   (MGI Ref ID J:65486)
  • increased circulating insulin level
    • homozygotes exhibit a 50 fold range in fasting insulin (2.5-125 ng/ml)   (MGI Ref ID J:65486)

Lepob/Lepob

        BTBR.Cg-Lepob/WiscJ
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype
    • mice do not develop atherosclerosis   (MGI Ref ID J:185261)
  • growth/size/body phenotype
  • increased body weight
    • body weight is increased by 8 weeks of age as compared to heterozygotes and wild-type   (MGI Ref ID J:185261)
  • homeostasis/metabolism phenotype
  • albuminuria
    • albuminuria is detected as early as 8 weeks of age, progressing to a 10-fold difference by 20 weeks of age   (MGI Ref ID J:185261)
    • increased albumin creatinine ratio   (MGI Ref ID J:185261)
  • hyperglycemia
    • mice exhibit hyperglycemia by 8 weeks of age   (MGI Ref ID J:185261)
    • males progress to blood glucose levels of 399 +/- 38.8 mg/dl by 22 weeks of age   (MGI Ref ID J:185261)
    • females progress to blood glucose levels of 333 +/- 46.3 mg/dl by 22 weeks of age   (MGI Ref ID J:185261)
    • blood glucose levels are higher than obese mice on the C57BL/6 background   (MGI Ref ID J:185261)
    • hyperglycemia is more evident in males than females, but after a time delay, also occurs in females   (MGI Ref ID J:106121)
  • impaired glucose tolerance
    • inability to clear plasma glucose following an overnight fast   (MGI Ref ID J:106121)
  • increased blood urea nitrogen level
    • increased BUN levels in both male and female mice   (MGI Ref ID J:185261)
  • increased cholesterol level
    • increased cholesterol levels in both male and female mice   (MGI Ref ID J:185261)
  • increased circulating insulin level
    • mice are hyperinsulinemic by 6 weeks of age but levels decrease as glucose levels rise   (MGI Ref ID J:106121)
  • increased circulating triglyceride level   (MGI Ref ID J:106121)
    • increased serum triglyceride levels in both male and female mice   (MGI Ref ID J:185261)
  • insulin resistance
    • at 6 weeks of age, most females are insulin resistant; they are hyperinsulinemic while maintaining only moderately elevated glucose levels   (MGI Ref ID J:106121)
    • by 10 weeks of age, female mice are hyperglycemic while still maintaining high (but insufficient) levels of insulin   (MGI Ref ID J:106121)
    • by 14 weeks of age, many females have even lower plasma insulin and increasing plasma glucose levels   (MGI Ref ID J:106121)
    • males show a similar progression of insulin resistance as females but starting at an earlier age, showing high insulin and high glucose at 6 weeks of age   (MGI Ref ID J:106121)
  • renal/urinary system phenotype
  • abnormal podocyte morphology
    • reduced podocyte density   (MGI Ref ID J:185261)
    • reduced podocyte number   (MGI Ref ID J:185261)
  • albuminuria
    • albuminuria is detected as early as 8 weeks of age, progressing to a 10-fold difference by 20 weeks of age   (MGI Ref ID J:185261)
    • increased albumin creatinine ratio   (MGI Ref ID J:185261)
  • enlarged kidney
    • renal hypertrophy   (MGI Ref ID J:185261)
    • increased kidney weight
      • both sexes exhibit increased kidney weight as compared to wild-type   (MGI Ref ID J:185261)
      • kidney weight of males is increased compared to females   (MGI Ref ID J:185261)
  • expanded mesangial matrix
    • renal lesions are characterized by increased glomerular mesangial matrix accumulation   (MGI Ref ID J:185261)
  • glomerulosclerosis   (MGI Ref ID J:185261)
  • increased renal glomerulus basement membrane thickness
    • glomerular basement membrane thickness is increased by 18% as compared to wild-type   (MGI Ref ID J:185261)
  • mesangiolysis
    • mesangiolysis is observed in 8% of glomeruli 8 week old mice   (MGI Ref ID J:185261)
    • mesangiolysis increases with age reaching 33.1% by 22 weeks of age   (MGI Ref ID J:185261)
    • diffuse mesangial sclerosis   (MGI Ref ID J:185261)
  • renal glomerulus hypertrophy
    • increased glomerular size   (MGI Ref ID J:185261)
  • renal interstitial fibrosis
    • focal and mild interstitial fibrosis is observed in 12 week old mice   (MGI Ref ID J:185261)
    • interstitial collagen accumulation is increased at 24 weeks of age as compared to wild-type   (MGI Ref ID J:185261)
  • endocrine/exocrine gland phenotype
  • abnormal pancreatic islet morphology
    • architecture of islets is disrupted, with many noninsulin staining cells in the central core   (MGI Ref ID J:106121)
    • whole pancreas insulin content is reduced by 75-80% compared to mutants on the C57BL/6 background   (MGI Ref ID J:106121)
    • decreased pancreatic beta cell mass   (MGI Ref ID J:106121)
    • small pancreatic islets
      • many small islets that show poor insulin staining   (MGI Ref ID J:106121)
View Research Applications

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

Diabetes and Obesity Research
Hyperglycemia
Type 2 Diabetes (NIDDM)

Internal/Organ Research
Wound Healing
      delayed/impaired

Lepob related

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

Endocrine Deficiency Research
Adipose Defects
Hypothalamus/Pituitary Defects
Pancreas Defects

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency Associated with Other Defects

Internal/Organ Research
Adipose Defects

Metabolism Research

Reproductive Biology Research
Fertility Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Lepob
Allele Name obese
Allele Type Spontaneous
Common Name(s) ob; ob/ob;
Strain of OriginSTOCK Mlph a Tgfa Cdh23 Ednrb
Gene Symbol and Name Lep, leptin
Chromosome 6
Gene Common Name(s) LEPD; OB; OBS; ob; obese;
Molecular Note Sequencing of RT-PCR products revealed a nonsense mutation in codon 105 resulting from a C to T point mutation. The 16 kDa leptin protein, expressed predominantly in adipose tissue of normal mice, is missing from homozygous mutant mice (J:29081). [MGI Ref ID J:20512] [MGI Ref ID J:29081] [MGI Ref ID J:45748]

Genotyping

Genotyping Information

Genotyping Protocols

Lep ob, End Point Analysis
Lepob, Pyrosequencing
Lepob, Restriction Enzyme Digest


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Ewart-Toland A; Mounzih K; Qiu J; Chehab FF. 1999. Effect of the genetic background on the reproduction of leptin-deficient obese mice. Endocrinology 140(2):732-8. [PubMed: 9927300]  [MGI Ref ID J:52903]

Malik NM; Carter ND; Murray JF; Scaramuzzi RJ; Wilson CA; Stock MJ. 2001. Leptin requirement for conception, implantation, and gestation in the mouse. Endocrinology 142(12):5198-202. [PubMed: 11713215]  [MGI Ref ID J:94783]

Oler AT; Attie AD. 2008. A rapid, microplate SNP genotype assay for the leptinob allele. J Lipid Res 49(5):1126-9. [PubMed: 18272929]  [MGI Ref ID J:133040]

Additional References

Campfield LA; Smith FJ; Guisez Y; Devos R; Burn P. 1995. Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks [see comments] Science 269(5223):546-9. [PubMed: 7624778]  [MGI Ref ID J:29160]

Charlton HM. 1984. Mouse mutants as models in endocrine research. Q J Exp Physiol 69(4):655-76. [PubMed: 6393185]  [MGI Ref ID J:7702]

Coleman DL. 1973. Effects of parabiosis of obese with diabetes and normal mice. Diabetologia 9(4):294-8. [PubMed: 4767369]  [MGI Ref ID J:5401]

Coleman DL. 1982. Thermogenesis in diabetes-obesity syndromes in mutant mice. Diabetologia 22(3):205-11. [PubMed: 7075918]  [MGI Ref ID J:6756]

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]

Erickson JC; Hollopeter G; Palmiter RD. 1996. Attenuation of the obesity syndrome of ob/ob mice by the loss of neuropeptide Y. Science 274(5293):1704-7. [PubMed: 8939859]  [MGI Ref ID J:37106]

Halaas JL; Gajiwala KS; Maffei M; Cohen SL; Chait BT; Rabinowitz D; Lallone RL; Burley SK; Friedman JM. 1995. Weight-reducing effects of the plasma protein encoded by the obese gene [see comments] Science 269(5223):543-6. [PubMed: 7624777]  [MGI Ref ID J:29161]

Haluzik M; Colombo C; Gavrilova O; Chua S; Wolf N; Chen M; Stannard B; Dietz KR; Le Roith D; Reitman ML. 2004. Genetic background (C57BL/6J versus FVB/N) strongly influences the severity of diabetes and insulin resistance in ob/ob mice. Endocrinology 145(7):3258-64. [PubMed: 15059949]  [MGI Ref ID J:90742]

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

Kaplan ML; Trout JR; Leveille GA. 1976. Adipocyte size distribution in ob/ob mice during preobese and obese phases of development. Proc Soc Exp Biol Med 153(3):476-82. [PubMed: 1013161]  [MGI Ref ID J:5765]

MacDougald OA; Hwang CS; Fan H; Lane MD. 1995. Regulated expression of the obese gene product (leptin) in white adipose tissue and 3T3-L1 adipocytes. Proc Natl Acad Sci U S A 92(20):9034-7. [PubMed: 7568067]  [MGI Ref ID J:29081]

Nishina PM; Lowe S; Wang J; Paigen B. 1994. Characterization of plasma lipids in genetically obese mice: the mutants obese, diabetes, fat, tubby, and lethal yellow. Metabolism 43(5):549-53. [PubMed: 8177042]  [MGI Ref ID J:18161]

Pelleymounter MA; Cullen MJ; Baker MB; Hecht R; Winters D; Boone T; Collins F. 1995. Effects of the obese gene product on body weight regulation in ob/ob mice [see comments] Science 269(5223):540-3. [PubMed: 7624776]  [MGI Ref ID J:29162]

Trayhurn P; James WP. 1978. Thermoregulation and non-shivering thermogenesis in the genetically obese (ob/ob) mouse. Pflugers Arch 373(2):189-93. [PubMed: 565045]  [MGI Ref ID J:5958]

Trayhurn P; Thurlby PL; James WP. 1977. Thermogenic defect in pre-obese ob/ob mice. Nature 266(5597):60-2. [PubMed: 840297]  [MGI Ref ID J:12010]

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Yamada N; Katsuura G; Ochi Y; Ebihara K; Kusakabe T; Hosoda K; Nakao K. 2011. Impaired CNS leptin action is implicated in depression associated with obesity. Endocrinology 152(7):2634-43. [PubMed: 21521746]  [MGI Ref ID J:174906]

Yamauchi T; Kamon J; Waki H; Imai Y; Shimozawa N; Hioki K; Uchida S; Ito Y; Takakuwa K; Matsui J; Takata M; Eto K; Terauchi Y; Komeda K; Tsunoda M; Murakami K; Ohnishi Y; Naitoh T; Yamamura K; Ueyama Y; Froguel P; Kimura S; Nagai R; Kadowaki T. 2003. Globular adiponectin protected ob/ob mice from diabetes and ApoE-deficient mice from atherosclerosis. J Biol Chem 278(4):2461-8. [PubMed: 12431986]  [MGI Ref ID J:81727]

Yang G; Badeanlou L; Bielawski J; Roberts AJ; Hannun YA; Samad F. 2009. Central role of ceramide biosynthesis in body weight regulation, energy metabolism, and the metabolic syndrome. Am J Physiol Endocrinol Metab 297(1):E211-24. [PubMed: 19435851]  [MGI Ref ID J:151166]

Yang M; Sun J; Zhang T; Liu J; Zhang J; Shi MA; Darakhshan F; Guerre-Millo M; Clement K; Gelb BD; Dolgnov G; Shi GP. 2008. Deficiency and inhibition of cathepsin K reduce body weight gain and increase glucose metabolism in mice. Arterioscler Thromb Vasc Biol 28(12):2202-8. [PubMed: 18818416]  [MGI Ref ID J:159791]

Yang M; Zhang Y; Pan J; Sun J; Liu J; Libby P; Sukhova GK; Doria A; Katunuma N; Peroni OD; Guerre-Millo M; Kahn BB; Clement K; Shi GP. 2007. Cathepsin L activity controls adipogenesis and glucose tolerance. Nat Cell Biol 9(8):970-7. [PubMed: 17643114]  [MGI Ref ID J:129484]

Yang R; Sikka G; Larson J; Watts VL; Niu X; Ellis C; Miller K; Camara A; Reinke C; Savransky V; Polotsky VY; O'Donnell CP; Berkowitz DE; Barouch LA. 2011. Restoring Leptin Signaling Reduces Hyperlipidemia and Improves Vascular Stiffness Induced by Chronic Intermittent Hypoxia. Am J Physiol Heart Circ Physiol :. [PubMed: 21278136]  [MGI Ref ID J:168540]

Yang RY; Yu L; Graham JL; Hsu DK; Lloyd KC; Havel PJ; Liu FT. 2011. Ablation of a galectin preferentially expressed in adipocytes increases lipolysis, reduces adiposity, and improves insulin sensitivity in mice. Proc Natl Acad Sci U S A 108(46):18696-701. [PubMed: 21969596]  [MGI Ref ID J:180097]

Yang S; Lin HZ; Hwang J; Chacko VP; Diehl AM. 2001. Hepatic hyperplasia in noncirrhotic fatty livers: is obesity-related hepatic steatosis a premalignant condition? Cancer Res 61(13):5016-23. [PubMed: 11431335]  [MGI Ref ID J:70169]

Yang SQ; Lin HZ; Mandal AK; Huang J; Diehl AM. 2001. Disrupted signaling and inhibited regeneration in obese mice with fatty livers: implications for nonalcoholic fatty liver disease pathophysiology. Hepatology 34(4 Pt 1):694-706. [PubMed: 11584365]  [MGI Ref ID J:106504]

Ye H; Charpin-El Hamri G; Zwicky K; Christen M; Folcher M; Fussenegger M. 2013. Pharmaceutically controlled designer circuit for the treatment of the metabolic syndrome. Proc Natl Acad Sci U S A 110(1):141-6. [PubMed: 23248313]  [MGI Ref ID J:192622]

Ye J; Gao Z; Yin J; He Q. 2007. Hypoxia is a potential risk factor for chronic inflammation and adiponectin reduction in adipose tissue of ob/ob and dietary obese mice. Am J Physiol Endocrinol Metab 293(4):E1118-28. [PubMed: 17666485]  [MGI Ref ID J:125547]

Yeh JK; Evans JF; Niu QT; Aloia JF. 2006. A possible role for melanocortin peptides in longitudinal growth. J Endocrinol 191(3):677-86. [PubMed: 17170224]  [MGI Ref ID J:116680]

Yekollu SK; Thomas R; O'Sullivan B. 2011. Targeting curcusomes to inflammatory dendritic cells inhibits NF-kappaB and improves insulin resistance in obese mice. Diabetes 60(11):2928-38. [PubMed: 21885868]  [MGI Ref ID J:189374]

Yi CX; Tschop MH; Woods SC; Hofmann SM. 2012. High-fat-diet exposure induces IgG accumulation in hypothalamic microglia. Dis Model Mech 5(5):686-90. [PubMed: 22381575]  [MGI Ref ID J:187483]

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

Yin J; Gao Z; He Q; Zhou D; Guo Z; Ye J. 2009. Role of hypoxia in obesity-induced disorders of glucose and lipid metabolism in adipose tissue. Am J Physiol Endocrinol Metab 296(2):E333-42. [PubMed: 19066318]  [MGI Ref ID J:146063]

Yoon JC; Puigserver P; Chen G; Donovan J; Wu Z; Rhee J; Adelmant G; Stafford J; Kahn CR; Granner DK; Newgard CB; Spiegelman BM. 2001. Control of hepatic gluconeogenesis through the transcriptional coactivator PGC-1. Nature 413(6852):131-8. [PubMed: 11557972]  [MGI Ref ID J:120036]

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]

Yoshimoto S; Loo TM; Atarashi K; Kanda H; Sato S; Oyadomari S; Iwakura Y; Oshima K; Morita H; Hattori M; Honda K; Ishikawa Y; Hara E; Ohtani N. 2013. Obesity-induced gut microbial metabolite promotes liver cancer through senescence secretome. Nature 499(7456):97-101. [PubMed: 23803760]  [MGI Ref ID J:204711]

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

Yuan M; Konstantopoulos N; Lee J; Hansen L; Li ZW; Karin M; Shoelson SE. 2001. Reversal of obesity- and diet-induced insulin resistance with salicylates or targeted disruption of Ikkbeta. Science 293(5535):1673-7. [PubMed: 11533494]  [MGI Ref ID J:94827]

Zhang CY; Baffy G; Perret P; Krauss S; Peroni O; Grujic D; Hagen T; Vidal-Puig AJ; Boss O; Kim YB; Zheng XX; Wheeler MB; Shulman GI; Chan CB; Lowell BB. 2001. Uncoupling protein-2 negatively regulates insulin secretion and is a major link between obesity, beta cell dysfunction, and type 2 diabetes. Cell 105(6):745-55. [PubMed: 11440717]  [MGI Ref ID J:75196]

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

Zhang H; Shen WJ; Cortez Y; Kraemer FB; Azhar S. 2013. Nordihydroguaiaretic acid improves metabolic dysregulation and aberrant hepatic lipid metabolism in mice by both PPARalpha-dependent and -independent pathways. Am J Physiol Gastrointest Liver Physiol 304(1):G72-86. [PubMed: 23104557]  [MGI Ref ID J:194703]

Zhang J; Nakatsu Y; Shinjo T; Guo Y; Sakoda H; Yamamotoya T; Otani Y; Okubo H; Kushiyama A; Fujishiro M; Fukushima T; Tsuchiya Y; Kamata H; Iwashita M; Nishimura F; Katagiri H; Takahashi S; Kurihara H; Uchida T; Asano T. 2013. Par14 protein associates with insulin receptor substrate 1 (IRS-1), thereby enhancing insulin-induced IRS-1 phosphorylation and metabolic actions. J Biol Chem 288(28):20692-701. [PubMed: 23720771]  [MGI Ref ID J:201792]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

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

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2450.00
Animals Provided

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

Embryos

Price (US dollars $)
Frozen Embryo $1600.00

Standard Supply

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

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • Cryorecovery - Standard.
    Progeny testing is not required.
    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

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

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3185.00
Animals Provided

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

Embryos

Price (US dollars $)
Frozen Embryo $2080.00

Standard Supply

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

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • Cryorecovery - Standard.
    Progeny testing is not required.
    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

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

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

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

Control Information

  Control
   Untyped from the colony
   000662 C57BLKS/J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

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

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

No Liability

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

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

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

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


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