Description

Strain Information

Former Names B6.Cg-Dock7m +/+ Leprdb/J    (Changed: 14-MAY-09 ) B6.Cg-m +/+ Leprdb/J    (Changed: 28-APR-09 ) Type Congenic; Mutant Strain; Spontaneous Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Mating System Heterozygote x Heterozygote         (Female x Male)   01-JUN-09 Species laboratory mouse Background Strain C57BL/6J Donor Strain C57BLKS H2 Haplotype b Generation N5F84 (11-JAN-08)

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Appearance
black, fat
Related Genotype: a/a + Lepr^db/+ Lepr^db

Important Note
In the spring of 2009, The Jackson Laboratory eliminated the allele misty (m) from the 000697 colony. Misty was bred out at generation 86. It is distributed as B6.D2(BKS)-Dock7^m/J (009659).

Description
Mice homozygous for the diabetes spontaneous mutation (Lepr^db) become identifiably obese around 3 to 4 weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at four to eight weeks. Affected mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. On the C57BL/6 background there is compensatory hyperplasia of the islet B cells, and continued hyperinsulinemia throughout an 18- to 20-month life span. Wound healing is delayed and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Lepr^db/+) 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 Lepr^db may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in diabetic mice, interact with the Lepr^db mutation as modifiers of gender differences in obesity-induced diabetes susceptibility.

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 Lepr^db. Additional backgrounds available: C57BLKS/J-Dock7^m +/+ Lepr^db (000642), C57BL/6J-Dock7^m Lepr^db/+ + (000699), C57BLKS/J-Dock7^m Lepr^db/+ + (000700).

Control Information

	Control
	000664 C57BL/6J
Considerations for Choosing Controls

Related Strains

Strains carrying   Lepr^db allele

002048	B6 x C57BLKS-Dock7m Leprdb Myo15sh2-J/J
000699	B6.Cg-Dock7m Leprdb/+ +/J
000642	BKS.Cg-Dock7m +/+ Leprdb/J
000700	BKS.Cg-Dock7m Leprdb/+ +/J
008340	BKS.Cg-Leprdb Nos3tm1Unc/RhrsJ
001192	BKS.Cg-meaJ Leprdb +/+ + Dock7m/J
000707	CBA.Cg-Dock7m Leprdb/+ +/J
006654	FVB.BKS(D)-Leprdb/ChuaJ

View Strains carrying   Lepr^db     (8 strains)

Strains carrying other alleles of Lepr

000709	129P3/J-Leprdb-3J/J
008518	B6.129-Leprtm1Mgmj/J
008320	B6.129-Leprtm2(cre)Rck/J
008385	B6.129-Leprtm2Mgmj/J
008327	B6.129P2-Leprtm1Rck/J
004939	NOD/ShiLtJ-Leprdb-5J/LtJ
006846	STOCK Leprdb-9J/Jgn

View Strains carrying other alleles of Lepr     (7 strains)

Additional Web Information

Genetic Quality Control Annual Report

Phenotype

Phenotype Information

View Phenotypic Data

Phenotypic Data

Mouse Phenome Database

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms

Obesity - Models with phenotypic similarity to human disease where etiologies are distinct.2

2 Human genes are associated with this disease. Orthologs of those genes do not appear in the mouse genotype(s).

View Mammalian Phenotype Terms

Mammalian Phenotype Terms

      assigned by genotype

Lepr^db/Lepr^db

        B6.Cg-Dock7^m +/+ Lepr^db/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 Leprr^tm1Mgmj homozygotes
  • increase in body weight becomes apparent at 4-6 weeks of age
• behavior/neurological phenotype
• polyphagia (MGI Ref ID J:82334)
• reduced male mating frequency (MGI Ref ID J:6157)
• cardiovascular system phenotype
• abnormal myocardial fiber morphology (MGI Ref ID J:103063)
  • exhibit myocyte hypertrophy
• heart 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 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 circulating lipid level (MGI Ref ID J:18161)
  • HDL cholesterol and glucose levels increase concurrently
  • plasma lipid levels are similar 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 hormone level (MGI Ref ID J:6157)
  • female mice exhibit an increase in hypothalamic gonadotrophin releasing hormone compared to in wild-type mice
• decreased adiponectin level (MGI Ref ID J:115772)
  • decreased in serum
• increased circulating insulin level (MGI Ref ID J:82334)
• increased circulating leptin level (MGI Ref ID J:115772)
• 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
• reproductive system phenotype
• abnormal female reproductive system morphology (MGI Ref ID J:82334)
  • atrophy of the reproductive organs
• constricted vagina opening (MGI Ref ID J:6157)
• small uterus (MGI Ref ID J:6157)
• absent estrous cycle (MGI Ref ID J:6157)
  • mice exhibit diestrous vaginal acyclicity or occasional metestrous acyclicity
• absent estrus (MGI Ref ID J:82334)
  • females never show signs of vaginal oestrous
• anovulation (MGI Ref ID J:82334)
• female infertility (MGI Ref ID J:6157)
  • 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 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)

Lepr^db/Lepr^db

        involves: C57BL/6

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

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

Lepr^db/Lepr⁺

        B6.Cg-Dock7^m +/+ Lepr^db/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

Lepr^db/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

Lepr^db/Lepr⁺

        BKS.Cg-Dock7^m +/+ Lepr^db/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

Lepr^db/Lepr^db

        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
• obese (MGI Ref ID J:89242)
• 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 kidney 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

Lepr^db/Lepr^db

        FVB.BKS-Lepr^db

• 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-Lepr^db mice where glucose levels rarely exceed 250 mg/dl
  • fasting mice are hyperglycemic at 3 months of age, while obese B6.BKS-Lepr^db 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-Lepr^db 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-Lepr^db 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-Lepr^db females; at 5-7 months insulin levels (~500 ng/ml) are ~10-fold higher than levels in obese female obese B6.BKS-Lepr^db 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
• 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
• pancreatic islet hyperplasia (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
• digestive/alimentary phenotype
• 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
• pancreatic islet hyperplasia (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
• 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

Lepr^db/Lepr^db

        BKS.Cg-Dock7^m +/+ Lepr^db/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
• hyperglycemia (MGI Ref ID J:135864)
  • fasting blood glucose level is significantly higher than control at 26 weeks of age
• 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
• albuminuria (MGI Ref ID J:135864)
  • moderate albuminuria is observed at 26 weeks of age
• 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
• increased body weight (MGI Ref ID J:135864)
• 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
• abnormal mesangial cell (MGI Ref ID J:135864)
  • moderate mesangial expansion is observed in glomeruli at 26 weeks
• albuminuria (MGI Ref ID J:135864)
  • moderate albuminuria is observed at 26 weeks of age
• 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

Lepr^db/Lepr^db

        BKS.Cg-Dock7^m +/+ Lepr^db/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)

Lepr^db/Lepr^db

        involves: 129S2/SvPas * C57BL/6 * C57BLKS/J

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

Lepr^db/Lepr^db

        involves: C57BL/6 * C57BLKS/J

• growth/size phenotype
• decreased body length (MGI Ref ID J:142218)
• obese (MGI Ref ID J:142218)
  • early onset obesity starting from 4 weeks of age
• adipose tissue phenotype
• increased percent body fat (MGI Ref ID J:142218)
• homeostasis/metabolism phenotype
• abnormal body temperature regulation (MGI Ref ID J:142218)
  • thermoregulation in response to cold exposure is severely impaired compared to wild-type controls
• abnormal oxygen consumption (MGI Ref ID J:142218)
  • oxygen consumption normalized to lean mass is increased compared to wild-type controls but oxygen consumption normalized to metabolic size is decreased compared to wild-type controls
• decreased body temperature (MGI Ref ID J:142218)
• hyperglycemia (MGI Ref ID J:142218)
• impaired glucose tolerance (MGI Ref ID J:142218)
• increased circulating leptin level (MGI Ref ID J:142218)
• insulin resistance (MGI Ref ID J:142218)
• behavior/neurological phenotype
• hypoactivity (MGI Ref ID J:142218)
  • decreased activity in both the light and dark cycle
• polyphagia (MGI Ref ID J:142218)
• reproductive system phenotype
• female infertility (MGI Ref ID J:142218)

View Research Applications

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

Lepr^db 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

Genes & Alleles

Gene & Allele Information

Allele Symbol		Leprdb
Allele Name		diabetes
Allele Type		Spontaneous
Common Name(s)		Lepdb; Lepr-; Leprdb-1J; db; leprdb;
Strain of Origin		C57BLKS/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]

Genotyping

Genotyping Information

Genotyping Protocols

Lepr^db, Pyrosequencing
Lepr^db, Restriction Enzyme Digest

Helpful Links

Genotyping resources and troubleshooting

References

References

Selected Reference(s)

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

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]

Additional References

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

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

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

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

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

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

Lepr^db related

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Banks AS; Kon N; Knight C; Matsumoto M; Gutierrez-Juarez R; Rossetti L; Gu W; Accili D. 2008. SirT1 gain of function increases energy efficiency and prevents diabetes in mice. Cell Metab 8(4):333-41. [PubMed: 18840364]  [MGI Ref ID J:143422]

Barile GR; Pachydaki SI; Tari SR; Lee SE; Donmoyer CM; Ma W; Rong LL; Buciarelli LG; Wendt T; Horig H; Hudson BI; Qu W; Weinberg AD; Yan SF; Schmidt AM. 2005. The RAGE axis in early diabetic retinopathy. Invest Ophthalmol Vis Sci 46(8):2916-24. [PubMed: 16043866]  [MGI Ref ID J:103714]

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

Barouch LA; Berkowitz DE; Harrison RW; O'Donnell CP; Hare JM. 2003. Disruption of leptin signaling contributes to cardiac hypertrophy independently of body weight in mice. Circulation 108(6):754-9. [PubMed: 12885755]  [MGI Ref ID J:103063]

Barouch LA; Gao D; Chen L; Miller KL; Xu W; Phan AC; Kittleson MM; Minhas KM; Berkowitz DE; Wei C; Hare JM. 2006. Cardiac myocyte apoptosis is associated with increased DNA damage and decreased survival in murine models of obesity. Circ Res 98(1):119-24. [PubMed: 16339484]  [MGI Ref ID J:118064]

Bates SH; Dundon TA; Seifert M; Carlson M; Maratos-Flier E; Myers MG Jr. 2004. LRb-STAT3 signaling is required for the neuroendocrine regulation of energy expenditure by leptin. Diabetes 53(12):3067-73. [PubMed: 15561935]  [MGI Ref ID J:94585]

Bates SH; Kulkarni RN; Seifert M; Myers MG Jr. 2005. Roles for leptin receptor/STAT3-dependent and -independent signals in the regulation of glucose homeostasis. Cell Metab 1(3):169-78. [PubMed: 16054060]  [MGI Ref ID J:129847]

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]

Batra A; Pietsch J; Fedke I; Glauben R; Okur B; Stroh T; Zeitz M; Siegmund B. 2007. Leptin-dependent toll-like receptor expression and responsiveness in preadipocytes and adipocytes. Am J Pathol 170(6):1931-41. [PubMed: 17525261]  [MGI Ref ID J:122150]

Baumgart J; Wisniewski HG; Amlacher R; Zhukovskaya NV; Rentz E. 1989. Age-dependent antileukemic action and suppression of immune response by 1,4-benzoquinone-guanylhydrazone-thiosemicarbazone (ambazone) in mice. Neoplasma 36(4):393-400. [PubMed: 2770926]  [MGI Ref ID J:27903]

Begin-Heick N. 1992. Alpha-subunits of Gs and Gi in adipocyte plasma membranes of genetically diabetic (db/db) mice. Am J Physiol 263(1 Pt 1):C121-9. [PubMed: 1322037]  [MGI Ref ID J:2110]

Begin-Heick N. 1994. Liver beta-adrenergic receptors, G proteins, and adenylyl cyclase activity in obesity-diabetes syndromes. Am J Physiol 266(6 Pt 1):C1664-72. [PubMed: 8023896]  [MGI Ref ID J:18963]

Belke DD; Larsen TS; Gibbs EM; Severson DL. 2001. Glucose metabolism in perfused mouse hearts overexpressing human GLUT-4 glucose transporter. Am J Physiol Endocrinol Metab 280(3):E420-7. [PubMed: 11171596]  [MGI Ref ID J:134584]

Belmadani S; Palen DI; Gonzalez-Villalobos RA; Boulares HA; Matrougui K. 2008. Elevated epidermal growth factor receptor phosphorylation induces resistance artery dysfunction in diabetic db/db mice. Diabetes 57(6):1629-37. [PubMed: 18319304]  [MGI Ref ID J:136927]

Berk PD; Zhou S; Kiang C; Stump DD; Fan X; Bradbury MW. 1999. Selective up-regulation of fatty acid uptake by adipocytes characterizes both genetic and diet-induced obesity in rodents. J Biol Chem 274(40):28626-31. [PubMed: 10497230]  [MGI Ref ID J:57965]

Bjorbaek C; Elmquist JK; Frantz JD; Shoelson SE; Flier JS. 1998. Identification of SOCS-3 as a potential mediator of central leptin resistance. Mol Cell 1(4):619-25. [PubMed: 9660946]  [MGI Ref ID J:119803]

Boardman N; Hafstad AD; Larsen TS; Severson DL; Aasum E. 2009. Increased O2 cost of basal metabolism and excitation-contraction coupling in hearts from type 2 diabetic mice. Am J Physiol Heart Circ Physiol 296(5):H1373-9. [PubMed: 19286944]  [MGI Ref ID J:150888]

Bodary PF; Shen Y; Ohman M; Bahrou KL; Vargas FB; Cudney SS; Wickenheiser KJ; Myers MG Jr; Eitzman DT. 2007. Leptin regulates neointima formation after arterial injury through mechanisms independent of blood pressure and the leptin receptor/STAT3 signaling pathways involved in energy balance. Arterioscler Thromb Vasc Biol 27(1):70-6. [PubMed: 17095713]  [MGI Ref ID J:135034]

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]

Botusan IR; Sunkari VG; Savu O; Catrina AI; Grunler J; Lindberg S; Pereira T; Yla-Herttuala S; Poellinger L; Brismar K; Catrina SB. 2008. Stabilization of HIF-1alpha is critical to improve wound healing in diabetic mice. Proc Natl Acad Sci U S A 105(49):19426-31. [PubMed: 19057015]  [MGI Ref ID J:142033]

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

Boudina S; Sena S; Theobald H; Sheng X; Wright JJ; Hu XX; Aziz S; Johnson JI; Bugger H; Zaha VG; Abel ED. 2007. Mitochondrial energetics in the heart in obesity-related diabetes: direct evidence for increased uncoupled respiration and activation of uncoupling proteins. Diabetes 56(10):2457-66. [PubMed: 17623815]  [MGI Ref ID J:126567]

Brem H; Tomic-Canic M; Entero H; Hanflik AM; Wang VM; Fallon JT; Ehrlich HP. 2007. The synergism of age and db/db genotype impairs wound healing. Exp Gerontol 42(6):523-31. [PubMed: 17275236]  [MGI Ref ID J:123188]

Brezniceanu ML; Liu F; Wei CC; Chenier I; Godin N; Zhang SL; Filep JG; Ingelfinger JR; Chan JS. 2008. Attenuation of interstitial fibrosis and tubular apoptosis in db/db transgenic mice overexpressing catalase in renal proximal tubular cells. Diabetes 57(2):451-9. [PubMed: 17977949]  [MGI Ref ID J:132449]

Brown RL; Breeden MP; Greenhalgh DG. 1994. PDGF and TGF-alpha act synergistically to improve wound healing in the genetically diabetic mouse. J Surg Res 56(6):562-70. [PubMed: 8015312]  [MGI Ref ID J:19344]

Brun P; Castagliuolo I; Leo VD; Buda A; Pinzani M; Palu G; Martines D. 2007. Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis. Am J Physiol Gastrointest Liver Physiol 292(2):G518-25. [PubMed: 17023554]  [MGI Ref ID J:124815]

Buettner C; Pocai A; Muse ED; Etgen AM; Myers MG Jr; Rossetti L. 2006. Critical role of STAT3 in leptin's metabolic actions. Cell Metab 4(1):49-60. [PubMed: 16814732]  [MGI Ref ID J:129709]

Bunger L; Forsting J; McDonald KL; Horvat S; Duncan J; Hochscheid S; Baile CA; Hill WG; Speakman JR. 2003. Long-term divergent selection on fatness in mice indicates a regulation system independent of leptin production and reception. FASEB J 17(1):85-7. [PubMed: 12424222]  [MGI Ref ID J:118012]

Busso N; So A; Chobaz-Peclat V; Morard C; Martinez-Soria E; Talabot-Ayer D; Gabay C. 2002. Leptin signaling deficiency impairs humoral and cellular immune responses and attenuates experimental arthritis. J Immunol 168(2):875-82. [PubMed: 11777985]  [MGI Ref ID J:73743]

Calvert JW; Gundewar S; Jha S; Greer JJ; Bestermann WH; Tian R; Lefer DJ. 2008. Acute metformin therapy confers cardioprotection against myocardial infarction via AMPK-eNOS-mediated signaling. Diabetes 57(3):696-705. [PubMed: 18083782]  [MGI Ref ID J:132319]

Cao L; Lin EJ; Cahill MC; Wang C; Liu X; During MJ. 2009. Molecular therapy of obesity and diabetes by a physiological autoregulatory approach. Nat Med 15(4):447-54. [PubMed: 19270710]  [MGI Ref ID J:149375]

Carley AN; Severson DL. 2005. Fatty acid metabolism is enhanced in type 2 diabetic hearts. Biochim Biophys Acta 1734(2):112-26. [PubMed: 15904868]  [MGI Ref ID J:99066]

Chaput E; Saladin R; Silvestre M; Edgar AD. 2000. Fenofibrate and rosiglitazone lower serum triglycerides with opposing effects on body weight. Biochem Biophys Res Commun 271(2):445-50. [PubMed: 10799317]  [MGI Ref ID J:62209]

Chavey C; Lazennec G; Lagarrigue S; Clape C; Iankova I; Teyssier J; Annicotte JS; Schmidt J; Mataki C; Yamamoto H; Sanches R; Guma A; Stich V; Vitkova M; Jardin-Watelet B; Renard E; Strieter R; Tuthill A; Hotamisligil GS; Vidal-Puig A; Zorzano A; Langin D; Fajas L. 2009. CXC ligand 5 is an adipose-tissue derived factor that links obesity to insulin resistance. Cell Metab 9(4):339-49. [PubMed: 19356715]  [MGI Ref ID J:148169]

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]

Chen HC; Stone SJ; Zhou P; Buhman KK; Farese RV Jr. 2002. Dissociation of obesity and impaired glucose disposal in mice overexpressing acyl coenzyme a:diacylglycerol acyltransferase 1 in white adipose tissue. Diabetes 51(11):3189-95. [PubMed: 12401709]  [MGI Ref ID J:107180]

Chen J; Li H; Addabbo F; Zhang F; Pelger E; Patschan D; Park HC; Kuo MC; Ni J; Gobe G; Chander PN; Nasjletti A; Goligorsky MS. 2009. Adoptive transfer of syngeneic bone marrow-derived cells in mice with obesity-induced diabetes: selenoorganic antioxidant ebselen restores stem cell competence. Am J Pathol 174(2):701-11. [PubMed: 19147816]  [MGI Ref ID J:144186]

Cheng KK; Lam KS; Wang Y; Huang Y; Carling D; Wu D; Wong C; Xu A. 2007. Adiponectin-induced endothelial nitric oxide synthase activation and nitric oxide production are mediated by APPL1 in endothelial cells. Diabetes 56(5):1387-94. [PubMed: 17287464]  [MGI Ref ID J:122100]

Cheung W; Yu PX; Little BM; Cone RD; Marks DL; Mak RH. 2005. Role of leptin and melanocortin signaling in uremia-associated cachexia. J Clin Invest 115(6):1659-65. [PubMed: 15931394]  [MGI Ref ID J:99198]

Chiellini C; Costa M; Novelli SE; Amri EZ; Benzi L; Bertacca A; Cohen P; Del Prato S; Friedman JM; Maffei M. 2003. Identification of cathepsin K as a novel marker of adiposity in white adipose tissue. J Cell Physiol 195(2):309-21. [PubMed: 12652657]  [MGI Ref ID J:106181]

Chin M; Isono M; Isshiki K; Araki S; Sugimoto T; Guo B; Sato H; Haneda M; Kashiwagi A; Koya D. 2005. Estrogen and Raloxifene, a Selective Estrogen Receptor Modulator, Ameliorate Renal Damage in db/db Mice. Am J Pathol 166(6):1629-36. [PubMed: 15920148]  [MGI Ref ID J:98819]

Choe SS; Choi AH; Lee JW; Kim KH; Chung JJ; Park J; Lee KM; Park KG; Lee IK; Kim JB. 2007. Chronic activation of liver X receptor induces beta-cell apoptosis through hyperactivation of lipogenesis: liver X receptor-mediated lipotoxicity in pancreatic beta-cells. Diabetes 56(6):1534-43. [PubMed: 17369526]  [MGI Ref ID J:126465]

Choo HJ; Kim JH; Kwon OB; Lee CS; Mun JY; Han SS; Yoon YS; Yoon G; Choi KM; Ko YG. 2006. Mitochondria are impaired in the adipocytes of type 2 diabetic mice. Diabetologia 49(4):784-91. [PubMed: 16501941]  [MGI Ref ID J:107887]

Chu KY; Lau T; Carlsson PO; Leung PS. 2006. Angiotensin II type 1 receptor blockade improves beta-cell function and glucose tolerance in a mouse model of type 2 diabetes. Diabetes 55(2):367-74. [PubMed: 16443769]  [MGI Ref ID J:106880]

Chua S Jr; Liu SM; Li Q; Yang L; Thassanapaff VT; Fisher P. 2002. Differential beta cell responses to hyperglycaemia and insulin resistance in two novel congenic strains of diabetes (FVB- Lepr (db)) and obese (DBA- Lep (ob)) mice. Diabetologia 45(7):976-90. [PubMed: 12136396]  [MGI Ref ID J:78850]

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

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Song B; Scheuner D; Ron D; Pennathur S; Kaufman RJ. 2008. Chop deletion reduces oxidative stress, improves beta cell function, and promotes cell survival in multiple mouse models of diabetes. J Clin Invest 118(10):3378-89. [PubMed: 18776938]  [MGI Ref ID J:141141]

Song MJ; Kim KH; Yoon JM; Kim JB. 2006. Activation of Toll-like receptor 4 is associated with insulin resistance in adipocytes. Biochem Biophys Res Commun 346(3):739-45. [PubMed: 16781673]  [MGI Ref ID J:110515]

Song WC; Moore R; McLachlan JA; Negishi M. 1995. Molecular characterization of a testis-specific estrogen sulfotransferase and aberrant liver expression in obese and diabetogenic C57BL/KsJ-db/db mice. Endocrinology 136(6):2477-84. [PubMed: 7750469]  [MGI Ref ID J:25937]

Srinivasan S; Bolick DT; Hatley ME; Natarajan R; Reilly KB; Yeh M; Chrestensen C; Sturgill TW; Hedrick CC. 2004. Glucose regulates interleukin-8 production in aortic endothelial cells through activation of the p38 mitogen-activated protein kinase pathway in diabetes. J Biol Chem 279(30):31930-6. [PubMed: 15145956]  [MGI Ref ID J:91901]

Starkey JM; Haidacher SJ; LeJeune WS; Zhang X; Tieu BC; Choudhary S; Brasier AR; Denner LA; Tilton RG. 2006. Diabetes-induced activation of canonical and noncanonical nuclear factor-kappaB pathways in renal cortex. Diabetes 55(5):1252-9. [PubMed: 16644679]  [MGI Ref ID J:108658]

Stranahan AM; Arumugam TV; Cutler RG; Lee K; Egan JM; Mattson MP. 2008. Diabetes impairs hippocampal function through glucocorticoid-mediated effects on new and mature neurons. Nat Neurosci 11(3):309-17. [PubMed: 18278039]  [MGI Ref ID J:135292]

Stratigopoulos G; Padilla SL; Leduc CA; Watson E; Hattersley AT; McCarthy MI; Zeltser LM; Chung WK; Leibel RL. 2008. Regulation of Fto/Ftm gene expression in mice and humans. Am J Physiol Regul Integr Comp Physiol 294(4):R1185-96. [PubMed: 18256137]  [MGI Ref ID J:133509]

Su W; Guo Z; Randall DC; Cassis L; Brown DR; Gong MC. 2008. Hypertension and disrupted blood pressure circadian rhythm in Type 2 diabetic db/db mice. Am J Physiol Heart Circ Physiol 295(4):H1634-41. [PubMed: 18708447]  [MGI Ref ID J:141313]

Sun D; Li H; Zolkiewska A. 2008. The role of Delta-like 1 shedding in muscle cell self-renewal and differentiation. J Cell Sci 121(Pt 22):3815-23. [PubMed: 18957511]  [MGI Ref ID J:145774]

Surendran S; Kondapaka SB. 2005. Altered expression of neuronal nitric oxide synthase in the duodenum longitudinal muscle-myenteric plexus of obesity induced diabetes mouse: implications on enteric neurodegeneration. Biochem Biophys Res Commun 338(2):919-22. [PubMed: 16256069]  [MGI Ref ID J:102835]

Surendran S; Matalon R; Tyring SK. 2006. Upregulation of aspartoacylase activity in the duodenum of obesity induced diabetes mouse: Implications on diabetic neuropathy. Biochem Biophys Res Commun 345(3):973-5. [PubMed: 16707098]  [MGI Ref ID J:109646]

Surmi BK; Atkinson RD; Gruen ML; Coenen KR; Hasty AH. 2008. The role of macrophage leptin receptor in aortic root lesion formation. Am J Physiol Endocrinol Metab 294(3):E488-95. [PubMed: 18182468]  [MGI Ref ID J:133462]

Szabo C; Biser A; Benko R; Bottinger E; Susztak K. 2006. Poly(ADP-ribose) polymerase inhibitors ameliorate nephropathy of type 2 diabetic Leprdb/db mice. Diabetes 55(11):3004-12. [PubMed: 17065336]  [MGI Ref ID J:116551]

Tadayoni R; Paques M; Gaudric A; Vicaut E. 2003. Erythrocyte and leukocyte dynamics in the retinal capillaries of diabetic mice. Exp Eye Res 77(4):497-504. [PubMed: 12957148]  [MGI Ref ID J:85594]

Takahashi N; Waelput W; Guisez Y. 1999. Leptin is an endogenous protective protein against the toxicity exerted by tumor necrosis factor. J Exp Med 189(1):207-12. [PubMed: 9874578]  [MGI Ref ID J:52060]

Taleb S; Herbin O; Ait-Oufella H; Verreth W; Gourdy P; Barateau V; Merval R; Esposito B; Clement K; Holvoet P; Tedgui A; Mallat Z. 2007. Defective leptin/leptin receptor signaling improves regulatory T cell immune response and protects mice from atherosclerosis. Arterioscler Thromb Vasc Biol 27(12):2691-8. [PubMed: 17690315]  [MGI Ref ID J:147531]

Tang T; Reed MJ. 2001. Exercise adds to metformin and acarbose efficacy in db/db mice. Metabolism 50(9):1049-53. [PubMed: 11555837]  [MGI Ref ID J:71891]

Tang Y; Osawa H; Onuma H; Nishimiya T; Ochi M; Sugita A; Makino H. 2001. Phosphodiesterase 3B gene expression is enhanced in the liver but reduced in the adipose tissue of obese insulin resistant db/db mouse. Diabetes Res Clin Pract 54(3):145-55. [PubMed: 11689269]  [MGI Ref ID J:102595]

Teixeira SR; Tappenden KA; Erdman JW Jr. 2003. Altering dietary protein type and quantity reduces urinary albumin excretion without affecting plasma glucose concentrations in BKS.cg-m +Lepr db/+Lepr db (db/db) mice. J Nutr 133(3):673-8. [PubMed: 12612136]  [MGI Ref ID J:82219]

Tejada T; Catanuto P; Ijaz A; Santos JV; Xia X; Sanchez P; Sanabria N; Lenz O; Elliot SJ; Fornoni A. 2008. Failure to phosphorylate AKT in podocytes from mice with early diabetic nephropathy promotes cell death. Kidney Int 73(12):1385-93. [PubMed: 18385666]  [MGI Ref ID J:152875]

Thangarajah H; Yao D; Chang EI; Shi Y; Jazayeri L; Vial IN; Galiano RD; Du XL; Grogan R; Galvez MG; Januszyk M; Brownlee M; Gurtner GC. 2009. The molecular basis for impaired hypoxia-induced VEGF expression in diabetic tissues. Proc Natl Acad Sci U S A 106(32):13505-10. [PubMed: 19666581]  [MGI Ref ID J:151949]

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]

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Tong Z; Yang Z; Patel S; Chen H; Gibbs D; Yang X; Hau VS; Kaminoh Y; Harmon J; Pearson E; Buehler J; Chen Y; Yu B; Tinkham NH; Zabriskie NA; Zeng J; Luo L; Sun JK; Prakash M; Hamam RN; Tonna S; Constantine R; Ronquillo CC; Sadda S; Avery RL; Brand JM; London N; Anduze AL; King GL; Bernstein PS; Watkins S; Jorde LB; Li DY; Aiello LP; Pollak MR; Zhang K. 2008. Promoter polymorphism of the erythropoietin gene in severe diabetic eye and kidney complications. Proc Natl Acad Sci U S A 105(19):6998-7003. [PubMed: 18458324]  [MGI Ref ID J:134862]

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Wall SJ; Bevan D; Thomas DW; Harding KG; Edwards DR; Murphy G. 2002. Differential expression of matrix metalloproteinases during impaired wound healing of the diabetes mouse. J Invest Dermatol 119(1):91-8. [PubMed: 12164930]  [MGI Ref ID J:123421]

Wang F; Tong Q. 2008. Transcription factor PU.1 is expressed in white adipose and inhibits adipocyte differentiation. Am J Physiol Cell Physiol 295(1):C213-20. [PubMed: 18463231]  [MGI Ref ID J:138523]

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Wang Y; Zhou J; Minto AW; Hack BK; Alexander JJ; Haas M; Li YC; Heilig CW; Quigg RJ. 2006. Altered vitamin D metabolism in type II diabetic mouse glomeruli may provide protection from diabetic nephropathy. Kidney Int 70(5):882-91. [PubMed: 16820793]  [MGI Ref ID J:136491]

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Wolfrum C; Howell JJ; Ndungo E; Stoffel M. 2008. Foxa2 activity increases plasma high density lipoprotein levels by regulating apolipoprotein M. J Biol Chem 283(24):16940-9. [PubMed: 18381283]  [MGI Ref ID J:138581]

Won Hong S; Isono M; Chen S; Iglesias-De La Cruz MC; Han DC; Ziyadeh FN. 2001. Increased glomerular and tubular expression of transforming growth factor-beta1, its type II receptor, and activation of the Smad signaling pathway in the db/db mouse. Am J Pathol 158(5):1653-63. [PubMed: 11337363]  [MGI Ref ID J:69101]

Wright DE; Johnson MS; Arnett MG; Smittkamp SE; Ryals JM. 2007. Selective changes in nocifensive behavior despite normal cutaneous axon innervation in leptin receptor-null mutant (db/db) mice. J Peripher Nerv Syst 12(4):250-61. [PubMed: 18042135]  [MGI Ref ID J:150180]

Wysocki J; Ye M; Soler MJ; Gurley SB; Xiao HD; Bernstein KE; Coffman TM; Chen S; Batlle D. 2006. ACE and ACE2 activity in diabetic mice. Diabetes 55(7):2132-9. [PubMed: 16804085]  [MGI Ref ID J:111853]

Xie Z; Su W; Guo Z; Pang H; Post SR; Gong MC. 2006. Up-regulation of CPI-17 phosphorylation in diabetic vasculature and high glucose cultured vascular smooth muscle cells. Cardiovasc Res 69(2):491-501. [PubMed: 16336954]  [MGI Ref ID J:105719]

Xu A; Lam MC; Chan KW; Wang Y; Zhang J; Hoo RL; Xu JY; Chen B; Chow WS; Tso AW; Lam KS. 2005. Angiopoietin-like protein 4 decreases blood glucose and improves glucose tolerance but induces hyperlipidemia and hepatic steatosis in mice. Proc Natl Acad Sci U S A 102(17):6086-91. [PubMed: 15837923]  [MGI Ref ID J:98462]

Xu G; Kaneto H; Laybutt DR; Duvivier-Kali VF; Trivedi N; Suzuma K; King GL; Weir GC; Bonner-Weir S. 2007. Downregulation of GLP-1 and GIP receptor expression by hyperglycemia: possible contribution to impaired incretin effects in diabetes. Diabetes 56(6):1551-8. [PubMed: 17360984]  [MGI Ref ID J:126498]

Xu H; Barnes GT; Yang Q; Tan G; Yang D; Chou CJ; Sole J; Nichols A; Ross JS; Tartaglia LA; Chen H. 2003. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J Clin Invest 112(12):1821-30. [PubMed: 14679177]  [MGI Ref ID J:86952]

Xu J; Wang P; Li Y; Li G; Kaczmarek LK; Wu Y; Koni PA; Flavell RA; Desir GV. 2004. The voltage-gated potassium channel Kv1.3 regulates peripheral insulin sensitivity. Proc Natl Acad Sci U S A 101(9):3112-7. [PubMed: 14981264]  [MGI Ref ID J:88651]

Xu L; Rensing N; Yang XF; Zhang HX; Thio LL; Rothman SM; Weisenfeld AE; Wong M; Yamada KA. 2008. Leptin inhibits 4-aminopyridine- and pentylenetetrazole-induced seizures and AMPAR-mediated synaptic transmission in rodents. J Clin Invest 118(1):272-80. [PubMed: 18097472]  [MGI Ref ID J:130891]

Xu N; Nilsson-Ehle P; Hurtig M; Ahren B. 2004. Both leptin and leptin-receptor are essential for apolipoprotein M expression in vivo. Biochem Biophys Res Commun 321(4):916-21. [PubMed: 15358114]  [MGI Ref ID J:91738]

Yaguchi H; Togawa K; Moritani M; Itakura M. 2005. Identification of candidate genes in the type 2 diabetes modifier locus using expression QTL. Genomics 85(5):591-9. [PubMed: 15820311]  [MGI Ref ID J:97535]

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]

Yamashita H; Shao J; Qiao L; Pagliassotti M; Friedman JE. 2003. Effect of spontaneous gestational diabetes on fetal and postnatal hepatic insulin resistance in Lepr(db/+) mice. Pediatr Res 53(3):411-8. [PubMed: 12595588]  [MGI Ref ID J:102264]

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

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

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX1

Colony Maintenance

Breeding & Husbandry	When maintaining a live colony, these mice are bred as heterozygotes. Females homozygous for the mutation are infertile and males exhibit a reduced ability to mate.
Mating System	Heterozygote x Heterozygote         (Female x Male)   01-JUN-09
Diet Information	LabDiet® 5K52/5K67

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Standard Supply	Level 3. Up to 50 mice. Larger quantities or custom orders arranged upon request.
Supply Notes	Genomic DNA is available for this strain from the Mouse DNA Resource.
Important Note
In the spring of 2009, The Jackson Laboratory eliminated the allele misty (m) from the 000697 colony. Misty was bred out at generation 86. It is distributed as B6.D2(BKS)-Dock7m/J (009659).

Control Information

	Control
	000664 C57BL/6J
Considerations for Choosing Controls
USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
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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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"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.

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. 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.