Mice homozygous for the obese spontaneous mutation, (Lep^ob commonly referred to as ob or ob/ob) exhibit obesity hyperphagia, a diabetes-like syndrome of hyperglycemia, glucose intolerance, elevated plasma insulin, subfertility, impaired wound healing, and an increase in hormone production from both pituitary and adrenal glands. They are also hypometabolic and hypothermic. The obesity is characterized by an increase in both 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 mice carrying the diabetes mutation (Lepr^db), manifestation of the diabetic syndrome is strikingly dependent on genetic background. Lep^ob homozygotes on the BTBR background develop diabetes at six weeks (males), and eight weeks (females). Hyperglycemia is severe and progressive with a fasting plasma glucose of 400 mg/dl at 10 weeks (Stoehr et al., 2000). In contrast to homozygotes on the C57BL/6 background, BTBR homozygotes develop extreme obesity (Stoehr et al., 2004) and progressive hypertriglyceridemia (Lan et al., 2003). Hepatic lipogenesis is not increased and homozygotes do not develop hepatic steatosis (Lan et al., 2003). Males remain hyperinsulinemic although insulin levels and islet mass are much reduced (Stoehr personal communication). Two modifier loci (Mobe1, Mobe2, formerly, Moo1 and Moo2) regulate total fat mass. BTBR alleles of these loci semi-dominantly increase body mass (Stoehr et al., 2004).

Development

The obese mutation, ob, arose spontaneously at The Jackson Laboratory, Bar Harbor, Maine in 1949. The ob allele from B6.V-Lep^ob/J was introgressed into BTBR T⁺ tf/J using a marker-assisted backcrossing program for six generations at the University of Wisconsin, Madison (Stoehr, 2000). The donating investigator reports that no C57BL/6J alleles were detected with the exception of a 20 cM region on chromosome 6 flanking the leptin locus. Heterozygotes were intercrossed to produce mice homozygous for ob. This strain was donated to The Jackson Laboratory in 2003 and the backcross will be continued to N10.

Control Suggestions

Wild-type from the colony

Additional Information

Considerations for Choosing Controls

Selected References

Hudkins KL; Pichaiwong W; Wietecha T; Kowalewska J; Banas MC; Spencer MW; Muhlfeld A; Koelling M; Pippin JW; Shankland SJ; Askari B; Rabaglia ME; Keller MP; Attie AD; Alpers CE. 2010. BTBR Ob/Ob mutant mice model progressive diabetic nephropathy. J Am Soc Nephrol 21(9):1533-42. PubMed: 20634301 MGI: J:185261
Stoehr JP; Byers JE; Clee SM; Lan H; Boronenkov IV; Schueler KL; Yandell BS; Attie AD. 2004. Identification of major quantitative trait loci controlling body weight variation in ob/ob mice. Diabetes 53(1):245-9. PubMed: 14693723 MGI: J:87998
Stoehr JP; Nadler ST; Schueler KL; Rabaglia ME; Yandell BS; Metz SA; Attie AD. 2000. Genetic obesity unmasks nonlinear interactions between murine type 2 diabetes susceptibility loci Diabetes 49(11):1946-54. PubMed: 11078464 MGI: J:65486

View All References

Genetics

Lep^ob

Allele Symbol: Lep^ob

Allele Name	obese
Allele Type	Spontaneous (Null/Knockout)
Allele Synonym(s)	ob; ob/ob
Gene Symbol and Name	Lep, leptin
Gene Synonym(s)	LEPD; OB; OBS; ob; obese; obese
Strain of Origin	STOCK Mlph a Tgfa Cdh23 Ednrb
Chromosome	6
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).

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Cardiovascular Research
- Hypertriglyceridemia

Genotype: Lep^ob 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

Mammalian Phenotype Terms by Genotype

Genotype: Lep^ob/Lep^ob
BTBR.Cg-Lep^ob/WiscJ

cardiovascular system phenotype

cardiovascular system phenotype
- mice do not develop atherosclerosis

hypotension

growth/size/body region phenotype

increased body weight
- body weight is increased by 8 weeks of age as compared to heterozygotes and wild-type

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
- increased albumin creatinine ratio

hyperglycemia
- Background Sensitivity - blood glucose levels are higher than obese mice on the C57BL/6 background
- females progress to blood glucose levels of 333 +/- 46.3 mg/dl by 22 weeks of age
- hyperglycemia is more evident in males than females, but after a time delay, also occurs in females
- males progress to blood glucose levels of 399 +/- 38.8 mg/dl by 22 weeks of age
- mice exhibit hyperglycemia by 8 weeks of age

impaired glucose tolerance
- inability to clear plasma glucose following an overnight fast

increased blood urea nitrogen level
- increased BUN levels in both male and female mice

increased cholesterol level
- increased cholesterol levels in both male and female mice

increased circulating insulin level
- mice are hyperinsulinemic by 6 weeks of age but levels decrease as glucose levels rise

increased circulating triglyceride level
- increased serum triglyceride levels in both male and female mice

insulin resistance
- at 6 weeks of age, most females are insulin resistant; they are hyperinsulinemic while maintaining only moderately elevated glucose levels
- by 10 weeks of age, female mice are hyperglycemic while still maintaining high (but insufficient) levels of insulin
- by 14 weeks of age, many females have even lower plasma insulin and increasing plasma glucose levels
- 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

renal/urinary system phenotype

abnormal podocyte morphology
- reduced podocyte density
- reduced podocyte number

albuminuria
- albuminuria is detected as early as 8 weeks of age, progressing to a 10-fold difference by 20 weeks of age
- increased albumin creatinine ratio

enlarged kidney
- renal hypertrophy

expanded mesangial matrix
- renal lesions are characterized by increased glomerular mesangial matrix accumulation

glomerulosclerosis

increased kidney weight
- both sexes exhibit increased kidney weight as compared to wild-type
- kidney weight of males is increased compared to females

increased renal glomerulus basement membrane thickness
- glomerular basement membrane thickness is increased by 18% as compared to wild-type

mesangiolysis
- diffuse mesangial sclerosis
- mesangiolysis increases with age reaching 33.1% by 22 weeks of age
- mesangiolysis is observed in 8% of glomeruli 8 week old mice

renal glomerulus hypertrophy
- increased glomerular size

renal interstitial fibrosis
- focal and mild interstitial fibrosis is observed in 12 week old mice
- interstitial collagen accumulation is increased at 24 weeks of age as compared to wild-type

endocrine/exocrine gland phenotype

abnormal pancreatic islet morphology
- architecture of islets is disrupted, with many noninsulin staining cells in the central core
- whole pancreas insulin content is reduced by 75-80% compared to mutants on the C57BL/6 background

decreased pancreatic beta cell mass

small pancreatic islets
- many small islets that show poor insulin staining

Genotype: Lep^ob/Lep^ob
BTBR.Cg-Lep^ob

homeostasis/metabolism phenotype

hyperglycemia
- Background Sensitivity - homozygotes exhibit severe, progressive hyperglycemia between 10-14 weeks of age as compared to the mild, transient hyperglycemia observed on the C57BL/6 background

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

Genotype: Lep^ob/Lep⁺
involves: C57BL/6J

skeleton phenotype

increased bone mass
- increased bone mass even on a low fat diet to delay obesity

Genotype: Lep^ob/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

Genotype: Lep^ob/Lep^ob
B6.Cg-Lep^ob/J

growth/size/body region phenotype

abnormal body weight
- body weight reduced by treatment with Leptin
- treatment with triiodothyronine significantly reduces body weight relative to the reduction seen in controls

increased body weight

increased growth rate
- mice reach 60-70 g by 10 months of age

obese
- 12-week old males are obese
- develop progressive obesity

renal/urinary system phenotype

abnormal urine catecholamine level
- less epinephrine in the urine of ad libitum fed mice
- males show elevated levels of dopamine in urine
- urine levels of norepinephrine only slightly elevated

abnormal urine homeostasis
- males show elevated levels of serotonin and 5'hydroxyindolineacetic acid in urine

immune system phenotype

decreased NK cell number
- reduced numbers can be restored by treatment with leptin

lung inflammation
- ozone induces a nonsignificant elevation of TNFR2 levels
- ozone induces significantly elevated levels of TNFR1

neoplasm

increased metastatic potential
- increased metastasis to the lung of both melanoma cell lines and lung cancer cell lines initially injected in the tail vein
- leptin reduces the level of metastasis

hematopoietic system phenotype

decreased NK cell number
- reduced numbers can be restored by treatment with leptin

nervous system phenotype

abnormal sympathetic nervous system physiology

liver/biliary system phenotype

abnormal liver weight
- treatment with triiodothyronine significantly reduces relative and absolute liver weight

integument phenotype

abnormal pain threshold

allodynia
- epineural application of leptin treated peritoneal macrophage induces tactile allodynia
- resistant to tactile allodynia caused by partial sciatic nerve ligation

hyperalgesia
- display thermal hyperalgesia after partial sciatic nerve ligation

skeleton phenotype

abnormal bone marrow morphology
- bone marrow is almost completely replaced with mature adipocytes

homeostasis/metabolism phenotype

abnormal circulating cholesterol level

abnormal circulating glucose level

abnormal oxygen consumption
- increased by treatment with triiodothyronine
- insulin stimulated oxygen consumption by the soleus muscle is little affected by triiodothyronine
- oxygen consumption about 2/3 that observed in controls

abnormal protein level
- total body protein increased by treatment with triiodothyronine
- total body protein lower than in controls

abnormal urine catecholamine level
- less epinephrine in the urine of ad libitum fed mice
- males show elevated levels of dopamine in urine
- urine levels of norepinephrine only slightly elevated

abnormal urine homeostasis
- males show elevated levels of serotonin and 5'hydroxyindolineacetic acid in urine

decreased body temperature
- body temperature is maintained a basal level when the ambient temperature is gradually reduced to 4C

decreased circulating glucose level
- 4 weeks' treatment with Adipor2-ASO (antisense oligonucleotide) significantly reduces plasma glucose levels in fed mice
- after feeding, serum glucose levels are more than 30% lower than in wild-type mice
- when treated with AdipoR2-ASO, mice exhibit a decrease in plasma glucose level

decreased insulin secretion
- leptin-treated islet cells exhibit decreased insulin secretion compared to similarly treated wild-type islets

decreased oxygen consumption
- in the epididymal and brown fat pads

hyperglycemia
- Background Sensitivity - blood glucose levels are lower than obese mice on the BTBR background
- Background Sensitivity - homozygotes exhibit a mild, transient hyperglycemia between 10-14 weeks of age as compared to the severe, progressive hyperglycemia observed on the BTBR background
- blood sugar peaks at 2-3 months
- males exhibit elevated blood glucose levels (254.4 +/-33.7 mg/dl) as compared to wild-type between 20-22 weeks of age
- mice infrequently transition to severe hyperglycemia
- returns to normal by 4-5 months of age
- serum glucose is 320 mg/dl compared to 134 mg/dl in wild-type controls
- transient hyperglycemia

hypoglycemia
- older mice are usually hypoglycemic

impaired glucose tolerance
- following an acute intraperitoneal glucose injection, the post-challenge glucose level remained elevated up to 120 min compared to controls, indicating glucose intolerance
- glucose intolerance which improved when treated with rosiglitazone

increased circulating HDL cholesterol level

increased circulating LDL cholesterol level

increased circulating VLDL cholesterol level

increased circulating cholesterol level
- fasting plasma total cholesterol concentration is increased 2-3 fold over controls

increased circulating insulin level
- at 2 weeks, insulin levels are increased 2.5-fold compared to in wild-type mice
- however, mice treated with isoproterenol exhibit lowered serum levels of insulin
- insulin levels increase rapidly to over 50X normal controls
- seen in 12-week old males
- serum insulin is 41.5 ng/ml compared to 0.8 ng/ml in wild-type

increased circulating triglyceride level
- seen in 12-week old males
- triglyceride levels are elevated 1.5- to 2-fold

increased insulin secretion
- insulin content in the pancreata is increased compared to in wild-type mice

increased oxygen consumption
- in the liver

insulin resistance

cardiovascular system phenotype

abnormal myocardial fiber morphology
- cardiomyocytes exhibit a significantly enlarged cross-sectional area
- 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
- exhibit myocyte hypertrophy, with increased myocyte diameter and distorted nuclear architecture

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 levelse, and significantly higher oxygen levels

decreased cardiac muscle contractility
- cardiomyocytes exhibit a reduced contractile capacity
- decreased peak shortening
- elevated resting peak calcium ion concentration
- 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
- prolonged relengthening
- slowed intracellular calcium ion decay

enlarged myocardial fiber
- cardiomyocytes display larger resting cell length and cross-sectional area

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
- induced weight loss via leptin infusion, but not via caloric restriction, partially resolves the hypertrophy

muscle phenotype

abnormal muscle morphology
- muscle protein content is reduced

abnormal myocardial fiber morphology
- cardiomyocytes exhibit a significantly enlarged cross-sectional area
- 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
- exhibit myocyte hypertrophy, with increased myocyte diameter and distorted nuclear architecture

abnormal skeletal muscle fiber type ratio
- lower proportion of faster myosin heavy chain isoforms

decreased cardiac muscle contractility
- cardiomyocytes exhibit a reduced contractile capacity
- decreased peak shortening
- elevated resting peak calcium ion concentration
- 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
- prolonged relengthening
- slowed intracellular calcium ion decay

decreased skeletal muscle fiber size
- cross-sectional area of muscle fibers is generally smaller

decreased skeletal muscle mass
- mean muscle mass consistently less than controls but magnitude of difference is muscle specific

enlarged myocardial fiber
- cardiomyocytes display larger resting cell length and cross-sectional area

adipose tissue phenotype

abnormal epididymal fat pad morphology
- adipocyte size remains larger after treatment with triiodothyronine relative to controls
- treatment with triiodothyronine significantly reduces epididymal fat pad weight relative to the degree of reduction seen in controls

decreased white fat cell number
- treatment with triiodothyronine reduces adipocyte numbers
- treatment with triiodothyronine significantly reduces adipocyte numbers relative to the degree of reduction seen in controls

increased fat cell size

increased interscapular fat pad weight
- affected less by treatment with triiodothyronine than controls
- brown adipocyte numbers are normal
- greater weight than for controls

increased percent body fat/body weight
- mice have fat mass of ~42 g compared to ~3 g in wild-type at 16 weeks

behavior/neurological phenotype

abnormal food intake

abnormal frequency of paradoxical sleep
- increased REM in dark phase
- reduced REM in light phase

abnormal pain threshold

abnormal sleep pattern
- additional sleep primarily in the dark phase
- increased non-REM sleep time
- increased total sleep time in a 24 hour period
- recovery from sleep deprivation involves increased duration of non-REM bouts rather than increased number of bouts as seen in controls

allodynia
- epineural application of leptin treated peritoneal macrophage induces tactile allodynia
- resistant to tactile allodynia caused by partial sciatic nerve ligation

decreased food intake
- food intake is reduced by Leptin treatment

fragmentation of sleep/wake states
- more arousals
- shorter wake periods
- sleep more fragmented

hyperalgesia
- display thermal hyperalgesia after partial sciatic nerve ligation

hypoactivity
- less wheel running activity
- more wheel running activity in light phase and less in dark phase
- significantly reduced activity relative to wild-type controls

increased food intake
- increased food intake when ambient temperature drops from 28 to 21C

polyphagia
- mice eat 70% more than wild-type controls

reproductive system phenotype

female infertility
- females do not produce litters

respiratory system phenotype

lung inflammation
- ozone induces a nonsignificant elevation of TNFR2 levels
- ozone induces significantly elevated levels of TNFR1

endocrine/exocrine gland phenotype

abnormal pancreatic beta cell physiology
- Background Sensitivity - less beta cell degranulation than seen on the "BKS" background

decreased insulin secretion
- leptin-treated islet cells exhibit decreased insulin secretion compared to similarly treated wild-type islets

enlarged pancreatic islets

increased insulin secretion
- insulin content in the pancreata is increased compared to in wild-type mice

Genotype: Lep^ob/Lep^ob
B6.Cg-Lep^ob/JRj

cellular phenotype

abnormal cell cycle
- hepatocytes accumulate in G2 phase in cultures at 60 hours after plating indicating a G2/M arrest
- hepatocytes accumulate in S phase at late time points during culture compared to control hepatocytes which exit S phase
- treatment with the antioxidant NAC reduces accumulation of BrdU at 60 hours after plating, indicating normal progression through the cell cycle

oxidative stress
- long-term administration of NAC alleviates oxidative stress in the liver parenchyma
- markers of oxidative stress are detectable in hepatocytes both in vitro and in vivo
- treatment with the antioxidant NAC impairs the accumulation of ROS with no impact on cell viability

liver/biliary system phenotype

abnormal hepatocyte physiology
- binuclear fraction of hepatocytes is lower in the liver parenchyma
- liver contains highly polyploid mononuclear hepatocytes which are infrequently seen in wild-type liver
- livers are enriched in hepatocytes with high DNA content compared to controls
- the mononuclear diploid (2n) hepatocyte population is lower in the mutant liver than in wild-type liver while mononuclear tetraploid hepatocytes are enriched in the mutant liver
- treatment with the antioxidant NAC restores a normal ploidy profile in mutant cultures

Genotype: Lep^ob/Lep^ob
B6.Cg-Lep^ob/OlaHsd

digestive/alimentary phenotype

abnormal digestive system physiology
- transepithelial resistance in the epithelium is reduced, indictive of a disrupted mucosal barrier function

abnormal intestinal epithelium morphology
- reduced levels of occludin in intestinal sections
- zonula occludens 1 has a discontinuous distribution

immune system phenotype

abnormal acute inflammation
- higher levels of endotoxin are found in portal blood (entotoxemia)

abnormal chemokine secretion
- increased release of monocyte chemo attractant protein by hepatic stellate cells

increased interleukin-6 secretion
- increased release by hepatic stellate cells

increased susceptibility to endotoxin shock
- increased succeptibility of hepatic stellate cells to LPS

liver inflammation

liver/biliary system phenotype

liver inflammation

Genotype: Lep^ob/Lep^ob
involves: 129/Sv * C57BL/6

homeostasis/metabolism phenotype

abnormal lipid level
- sphingomeylin and antioxidant ethanolamine plasmlogen are markedly decreased

increased circulating insulin level
- at 4 and 16 weeks of age

increased insulin secretion
- at 16 weeks of age

insulin resistance
- at 16 weeks

endocrine/exocrine gland phenotype

abnormal pancreatic islet morphology
- at 16 weeks, increased islet-to-pancreases volume ratios
- at 16 weeks, islet insulin content is 30-fold greater than in Pparg^tm1Avb Lep^ob homozygotes

enlarged pancreatic islets

increased insulin secretion
- at 16 weeks of age

increased pancreatic islet number

behavior/neurological phenotype

hypoactivity
- at 20 weeks, mice have decreased locomotor activity compared to wild-type

polyphagia
- hyperphagic

growth/size/body region 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

adipose tissue phenotype

increased percent body fat/body weight
- 40% increase compared to wild-type at 20 weeks

liver/biliary system phenotype

hepatic steatosis

Genotype: Lep^ob/Lep^ob
involves: STOCK Mlph^ln a Tgfa^wa1 Cdh23^v Ednrb^s

growth/size/body region phenotype

decreased body length
- expansive hind quarters
- first noticeable at 4-6 weeks of age
- short body
- square shape

increased body weight

increased growth rate
- begin to gain weight rapidly by 4-6 weeks of age
- weigh 75-90g at 10 months
- weigh twice as much as controls at 3 months of age

cardiovascular system phenotype

abnormal arteriole morphology
- basal arteriolar diameter is greater than controls
- potassium-ATP channel inhibition eliminates diameter difference from controls

abnormal vascular wound healing
- neointimal area increased by leptin injection or adenoviral leptin treatment
- reduced neointimal area relative to controls 4 weeks after femoral artery injury
- vascular smooth muscle proliferation significantly reduced

altered response to myocardial infarction
- mice exhibit a significant decline in cardiac function, and increase in apoptosis and necrosis, and elevated reactive oxygen species generation after myocardial ischemia/reperfusion injury

immune system phenotype

abnormal microglial cell physiology
- 30-40% as many activated microglia 5 days after kainic acid treatment as for controls
- migrate normally to injury sites but do not proliferate

decreased circulating tumor necrosis factor level
- 48% of control levels after kainate injection

limbs/digits/tail phenotype

short femur

short humerus

embryo phenotype

abnormal embryonic neuroepithelium morphology
- cell proliferation is lower at E14 and E16
- significantly fewer cells at E16 and E18 but not at E14

decreased embryonic neuroepithelium thickness
- thin at E18

hematopoietic system phenotype

abnormal microglial cell physiology
- 30-40% as many activated microglia 5 days after kainic acid treatment as for controls
- migrate normally to injury sites but do not proliferate

liver/biliary system phenotype

decreased liver triglyceride level
- lower level than wild-type after 36 hour fasting in 7-week-old mice.

decreased susceptibility to hepatic steatosis
- after 36 hour fasting in 7-week-old mice

increased liver triglyceride level
- double the control littermate's triglyceride level in 7 to 14 weeks old mice

behavior/neurological phenotype

polyphagia
- hyperphagia

homeostasis/metabolism phenotype

abnormal glucose homeostasis

abnormal hormone level
- increased beta endorphin levels
- increased levels of melanocyte stimulating hormone

abnormal vascular wound healing
- neointimal area increased by leptin injection or adenoviral leptin treatment
- reduced neointimal area relative to controls 4 weeks after femoral artery injury
- vascular smooth muscle proliferation significantly reduced

altered response to myocardial infarction
- mice exhibit a significant decline in cardiac function, and increase in apoptosis and necrosis, and elevated reactive oxygen species generation after myocardial ischemia/reperfusion injury

decreased body temperature
- mice have a lower basal body temperature than controls

decreased circulating tumor necrosis factor level
- 48% of control levels after kainate injection

decreased liver triglyceride level
- lower level than wild-type after 36 hour fasting in 7-week-old mice.

hyperglycemia
- transient hyperglycemia

impaired adaptive thermogenesis
- 60 minute exposure of 17 day old mice to 4C results in a marked drop in body temperature
- extreme cold susceptibility
- mice acclimated to 12C before exposure survive better to 4C exposure than un-acclimated controls
- mice moved directly to 4C from 21C become hypothermic and die

impaired glucose tolerance

increased adrenocorticotropin level
- increased pituitary ACTH

increased circulating insulin level

increased liver triglyceride level
- double the control littermate's triglyceride level in 7 to 14 weeks old mice

endocrine/exocrine gland phenotype

abnormal gland physiology

abnormal pancreatic beta cell morphology

decreased activity of thyroid

hypersecretion of corticosterone
- increased glucocorticoids from the adrenal

increased pancreatic beta cell mass
- increased size

increased pancreatic beta cell number

adipose tissue phenotype

abnormal fat cell morphology
- hyperplasia

increased fat cell size

skeleton phenotype

abnormal long bone epiphyseal plate morphology
- breakage at the chondro-osseous junction
- failure at a force of 4.9 Newtons as compared to 8.4 Newtons in controls
- less organized loose reticular distribution of collagen fibrils
- more fragile than controls
- reduced expression of "type-X" collagen

abnormal long bone epiphyseal plate proliferative zone
- column structure is disturbed
- poor alignment

abnormal long bone hypertrophic chondrocyte zone
- column structure is disturbed
- increased numbers of apoptotic chondrocytes
- mostly mineralized as compared to less than 50% mineralized in controls
- poor alignment

decreased bone mass
- reduced bone mass

decreased length of long bones

short femur

short humerus

reproductive system phenotype

female infertility
- homozygous females fail to ovulate

infertility

male infertility
- all older males are sterile

reduced male fertility
- only 20% of young males are fertile

nervous system phenotype

abnormal cortical plate morphology
- fewer cells in the cortical plate at E18

abnormal embryonic neuroepithelium morphology
- cell proliferation is lower at E14 and E16
- significantly fewer cells at E16 and E18 but not at E14

abnormal microglial cell physiology
- 30-40% as many activated microglia 5 days after kainic acid treatment as for controls
- migrate normally to injury sites but do not proliferate

decreased embryonic neuroepithelial cell proliferation
- cell proliferation is lower at E14 and E16

decreased embryonic neuroepithelium thickness
- thin at E18

Genotype: Lep^ob/Lep^ob
involves: 129X1/SvJ * C57BL/6

growth/size/body region 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)

increased body weight
- higher than wild-type

integument phenotype

abnormal branching of the mammary ductal tree
- in virgin females, no ductal development occurs

homeostasis/metabolism phenotype

abnormal circulating hormone level

abnormal circulating pancreatic peptide level
- plasma levels of pancreatic polypeptide (PP) are strongly reduced compared to wild-type

decreased circulating testosterone level
- level is markedly decreased compared to wild-type or Lep heterozygotes
- significantly lower (4.2 nmol/l) compared to wild-type (14.2 nmol/l)

hyperglycemia

increased circulating cholesterol level
- 5.74 mmol/l vs 3.54 mmol/l in wild-type

increased circulating corticosterone level
- mice display hypercorticosteronemia compared to wild-type
- mice display hypercorticosteronemia compared to wild-type, Npy2r^tm1.1Hhz homozygotes, or Npy2r, Lep double mutants

increased circulating insulin level
- hyperinsulinemic compared to wild-type
- level is significantly increased over wild-type

increased circulating leptin level
- level is significantly increased over wild-type

increased circulating triglyceride level
- 2.48 mmol/l vs 1.62 mmol/l in wild-type

endocrine/exocrine gland phenotype

abnormal branching of the mammary ductal tree
- in virgin females, no ductal development occurs

abnormal ovarian folliculogenesis
- ovaries have very few primary or secondary follicles

absent corpus luteum
- no corpora lutea develops properly in ovary

decreased seminal vesicle weight
- weight of gland is significantly lower than wild-type or heterozygotes

decreased testis weight
- testes weigh 0.19 g compared to 0.33 g in wild-type
- testis weight is significantly lower than in Lep^ob heterozygotes or Lep, Ppyr1 double null mice

increased pancreas weight
- 0.41 g vs 0.29 in wild-type

adipose tissue phenotype

abnormal adipose tissue amount
- combined white adipose tissue (WAT) mass is increased compared to wild-type

reproductive system phenotype

abnormal ovarian folliculogenesis
- ovaries have very few primary or secondary follicles

abnormal vagina orifice morphology
- vaginal opening is very small compared to wild-type

absent corpus luteum
- no corpora lutea develops properly in ovary

decreased seminal vesicle weight
- weight of gland is significantly lower than wild-type or heterozygotes

decreased testis weight
- testes weigh 0.19 g compared to 0.33 g in wild-type
- testis weight is significantly lower than in Lep^ob heterozygotes or Lep, Ppyr1 double null mice

female infertility
- homozygous females produce no litters

male infertility
- no males could produce offspring
- only one male tested was able to sire a litter

prolonged diestrus
- mice have diestrous-like swab until 9 weeks of age

prolonged estrous cycle
- beginning at 9 weeks of age, estrous cycles last 11-15 days

prolonged estrus
- beginning at 9 weeks of age, estrous-like cytology lasts 6-8 days

behavior/neurological phenotype

polyphagia

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)

liver/biliary system phenotype

increased liver weight
- 4.56 g vs 1.44 g in wild-type

renal/urinary system phenotype

increased kidney weight
- 0.54 g vs 0.41 g in wild-type

Genotype: Lep^ob/Lep^ob
involves: BTBR * C57BL/6 * V stock

endocrine/exocrine gland phenotype

decreased pancreatic beta cell number
- severely diabetic mice exhibit reduced numbers of beta cells

disorganized pancreatic islets
- moderate to severely diabetic F2 mice have no hyperplasia, but exhibit cellular disorganization and fibrosis
- severely diabetic F2 mice exhibit concavities with acinar tissue intrusions

pancreatic islet hyperplasia
- mildly diabetic F2 mice exhibit large numbers of hyperplastic pancreatic islets

homeostasis/metabolism phenotype

hyperglycemia
- homozygotes exhibit a 7.5 fold range in fasting glucose (100-750 mg/dl)

increased circulating insulin level
- homozygotes exhibit a 50 fold range in fasting insulin (2.5-125 ng/ml)

Genotype: Lep^ob/Lep^ob
involves: C57BL/6J

liver/biliary system phenotype

hepatic steatosis

increased liver weight

cardiovascular system phenotype

abnormal cardiovascular system physiology
- attenuated heart response to increased calcium
- oxygen consumption is elevated when perfused with glucose and palmitate
- oxygen consumption of the heart does not increase with an increased workload

abnormal retinal vasculature morphology
- neovascularization is significantly suppressed under standard oxygen conditions relative to controls

increased heart weight
- heart weight elevated relative to controls

muscle phenotype

abnormal muscle contractility
- basal calcium ion concentration increases sharply toward the end of a series of 50 tetanic contractions (single cell measures)
- number of tetani required to reduce force by 40% is significantly less than for controls

vision/eye phenotype

abnormal retinal vasculature morphology
- neovascularization is significantly suppressed under standard oxygen conditions relative to controls

nervous system phenotype

decreased nerve conduction velocity
- 16% lower motor nerve conduction velocity than controls
- hind limb sensory nerve conduction velocity reduced 22%

behavior/neurological phenotype

abnormal behavior
- faster in food finding trials relative to controls

hypoactivity

increased thermal nociceptive threshold
- 88% increased latency of hind-limb withdrawal from a heat stimulus

polyphagia
- mice eat twice as much as wild-type mice

immune system phenotype

abnormal osteoclast differentiation
- increased numbers of osteoclasts

cellular phenotype

abnormal osteoclast differentiation
- increased numbers of osteoclasts

abnormal respiratory electron transport chain
- increased ADP dependent mitochondrial respiration in glucose and palmitate perfused hearts
- mitochondrial respiration is inhibited in glucose perfused hearts
- mitochondrial respiration is uncoupled in glucose and palmitate perfused hearts

integument phenotype

abnormal epidermal layer morphology
- significant reduction in intraepidermal nerve fiber density

increased thermal nociceptive threshold
- 88% increased latency of hind-limb withdrawal from a heat stimulus

growth/size/body region phenotype

abnormal postnatal growth
- pair fed mice gain considerably more weight as fat than controls eating the same quantity of food
- pair fed mice gain less weight as protein than when feeding is unrestricted
- pair fed mice gain less weight than when feeding is unrestricted
- pair fed mice restrict food intake to that of controls

increased body length

increased lean body mass
- increase in lean mass at 8 and 16 weeks of age

obese
- increase in weight gain in a short period of time

endocrine/exocrine gland phenotype

abnormal colon goblet cell morphology
- increased number of mucus filled goblet cells in the colon

abnormal insulin secretion
- acetyl choline has a greater affect to lower the glucose induced threshold for insulin secretion
- lower threshold for glucose induced insulin secretion by beta cells

enlarged pancreatic islets
- increase in the size of islets of Langerhans and appearance of enormous islets in the pancreas of 30 week old mice

mortality/aging

postnatal lethality, incomplete penetrance
- 50 % higher postnatal death rate of males

homeostasis/metabolism phenotype

abnormal corticosterone level
- corticosterone response to stress greater than in controls
- diurnal variation greater than in controls

abnormal glucose homeostasis

abnormal hormone level

abnormal insulin secretion
- acetyl choline has a greater affect to lower the glucose induced threshold for insulin secretion
- lower threshold for glucose induced insulin secretion by beta cells

hyperglycemia

impaired glucose tolerance
- observed prior to any significant increase in body weight

increased adrenocorticotropin level
- levels in the pituitary are much higher than in pituitaries of controls

increased circulating corticosterone level
- severe

increased circulating insulin level

increased fasted circulating glucose level
- fasting mice show increased glucose levels at 6 weeks of age

insulin resistance
- in the insulin tolerance test, mice reduce their glucose levels within 30 min to about 80% compared to 50% in wild-type mice at 6 weeks of age
- mice do not respond to insulin in the insulin tolerance test at 15 weeks of age, indicating insulin resistance

skeleton phenotype

abnormal osteoclast differentiation
- increased numbers of osteoclasts

abnormal skeleton development
- rate of new bone formation increased at both 3 and 6 months

increased bone mass
- denser vertebrae and long bones at 6 months
- increased bone mass even on a low fat diet to delay obesity

osteopetrosis
- 2 fold increase in trabecular bone volume
- increased numbers of thick trabeculae at 3 and 6 months

hematopoietic system phenotype

abnormal osteoclast differentiation
- increased numbers of osteoclasts

adipose tissue phenotype

increased fat cell size
- increase in area size of epigonadal fat cells

increased gonadal fat pad weight
- increase in epigonadal fat tissue weight

increased inguinal fat pad weight

increased interscapular fat pad weight

increased percent body fat/body weight
- increase in fat mass at 8 and 16 weeks of age

digestive/alimentary phenotype

abnormal colon goblet cell morphology
- increased number of mucus filled goblet cells in the colon

abnormal intestinal mucosa morphology
- thick mucus gel covers the epithelium of the colon

Genotype: Lep^ob/Lep^ob
FVB.Cg-Lep^ob/Chua

homeostasis/metabolism phenotype

hyperglycemia
- mice are hyperglycemic like congenic FVB Lepr mice

increased circulating insulin level
- mice are hyperinsulinemic like congenic FVB Lepr^db mice

Genotype: Lep^ob/Lep^ob
involves: C57BL/6

homeostasis/metabolism phenotype

increased circulating HDL cholesterol level
- slightly elevated at 3 and 8 months of age

increased circulating cholesterol level
- seen at 3-4 months of age

increased circulating triglyceride level
- seen at 3-4 months of age

increased liver cholesterol level
- livers exhibit slightly, but significantly, higher levels of cholesterol

increased liver triglyceride level
- livers exhibit about 10x higher levels of triglyceride

liver/biliary system phenotype

increased liver cholesterol level
- livers exhibit slightly, but significantly, higher levels of cholesterol

increased liver triglyceride level
- livers exhibit about 10x higher levels of triglyceride

immune system phenotype

decreased CD4-positive, alpha beta T cell number

decreased T cell proliferation

decreased splenocyte number

hematopoietic system phenotype

decreased CD4-positive, alpha beta T cell number

decreased T cell proliferation

decreased splenocyte number

Genotype: Lep^ob/Lep^ob
B6.Cg-Lep^ob/JBomTac

homeostasis/metabolism phenotype

increased circulating triglyceride level
- 3-fold

Genotype: Lep^ob/Lep^ob
D2.Cg-Lep^ob/Chua

growth/size/body region phenotype

obese

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

increased circulating insulin level
- some mutant DBA/2J mice have high insulin levels compared to controls

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

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

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

Genotype: Lep^ob/Lep^ob
BKS.Cg-Lep^ob/J

mortality/aging

premature death

growth/size/body region phenotype

increased growth rate
- mice reach 45-55 g by 3-4 months of age
- slowly lose weight from 4 months on

homeostasis/metabolism phenotype

abnormal circulating cholesterol level

abnormal circulating glucose level

hyperglycemia
- blood sugar continues to rise
- blood sugar never returns to control levels
- stabilizes at around 400-500 mg/100 ml

increased circulating HDL cholesterol level

increased circulating LDL cholesterol level

increased circulating VLDL cholesterol level

increased circulating cholesterol level
- fasting plasma total cholesterol concentration is increased 2-3 fold over controls

increased circulating insulin level
- insulin levels increase only through the first 2 months
- levels drop back to normal

increased circulating triglyceride level
- triglyceride levels are elevated 1.5- to 2-fold

increased urine glucose level

endocrine/exocrine gland phenotype

abnormal pancreatic beta cell physiology
- Background Sensitivity - more beta cell degranulation than seen on the 'B6' background

small pancreatic islets
- after 2 months, islets become smaller and atrophic

renal/urinary system phenotype

increased urine glucose level

polyuria

References

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Additional References

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Ranheim T; Dumke C; Schueler KL; Cartee GD; Attie AD. 1997. Interaction between BTBR and C57BL/6J genomes produces an insulin resistance syndrome in (BTBR x C57BL/6J) F1 mice. Arterioscler Thromb Vasc Biol 17(11):3286-93. PubMed: 9409324 MGI: J:44943

Additional - Lep^ob related

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Also Known As: BTBR obese

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Lepob

Allele Symbol: Lepob

Disease Terms

Research Areas By Genotype

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

Genotype: Lepob related

Mammalian Phenotype Terms by Genotype

Genotype: Lepob/LepobBTBR.Cg-Lepob/WiscJ

cardiovascular system phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

renal/urinary system phenotype

endocrine/exocrine gland phenotype

Genotype: Lepob/LepobBTBR.Cg-Lepob

homeostasis/metabolism phenotype

Genotype: Lepob/Lep+involves: C57BL/6J

skeleton phenotype

Genotype: Lepob/Lep+involves: 129X1/SvJ * C57BL/6

liver/biliary system phenotype

Genotype: Lepob/LepobB6.Cg-Lepob/J

growth/size/body region phenotype

renal/urinary system phenotype

immune system phenotype

neoplasm

hematopoietic system phenotype

nervous system phenotype

liver/biliary system phenotype

integument phenotype

skeleton phenotype

homeostasis/metabolism phenotype

cardiovascular system phenotype

muscle phenotype

adipose tissue phenotype

behavior/neurological phenotype

reproductive system phenotype

respiratory system phenotype

endocrine/exocrine gland phenotype

Genotype: Lepob/LepobB6.Cg-Lepob/JRj

cellular phenotype

liver/biliary system phenotype

Genotype: Lepob/LepobB6.Cg-Lepob/OlaHsd

digestive/alimentary phenotype

immune system phenotype

liver/biliary system phenotype

Genotype: Lepob/Lepobinvolves: 129/Sv * C57BL/6

homeostasis/metabolism phenotype

endocrine/exocrine gland phenotype

behavior/neurological phenotype

growth/size/body region phenotype

adipose tissue phenotype

liver/biliary system phenotype

Genotype: Lepob/Lepobinvolves: STOCK Mlphln a Tgfawa1 Cdh23v Ednrbs

growth/size/body region phenotype

cardiovascular system phenotype

immune system phenotype

limbs/digits/tail phenotype

embryo phenotype

hematopoietic system phenotype

liver/biliary system phenotype

behavior/neurological phenotype

homeostasis/metabolism phenotype

endocrine/exocrine gland phenotype

adipose tissue phenotype

skeleton phenotype

reproductive system phenotype

nervous system phenotype

Genotype: Lepob/Lepobinvolves: 129X1/SvJ * C57BL/6

growth/size/body region phenotype

integument phenotype

homeostasis/metabolism phenotype

endocrine/exocrine gland phenotype

Lep^ob

Allele Symbol: Lep^ob

Genotype: Lep^ob related

Genotype: Lep^ob/Lep^ob
BTBR.Cg-Lep^ob/WiscJ

Genotype: Lep^ob/Lep^ob
BTBR.Cg-Lep^ob

Genotype: Lep^ob/Lep⁺
involves: C57BL/6J

Genotype: Lep^ob/Lep⁺
involves: 129X1/SvJ * C57BL/6

Genotype: Lep^ob/Lep^ob
B6.Cg-Lep^ob/J

Genotype: Lep^ob/Lep^ob
B6.Cg-Lep^ob/JRj

Genotype: Lep^ob/Lep^ob
B6.Cg-Lep^ob/OlaHsd

Genotype: Lep^ob/Lep^ob
involves: 129/Sv * C57BL/6

Genotype: Lep^ob/Lep^ob
involves: STOCK Mlph^ln a Tgfa^wa1 Cdh23^v Ednrb^s

Genotype: Lep^ob/Lep^ob
involves: 129X1/SvJ * C57BL/6

Genotype: Lep^ob/Lep^ob
involves: BTBR * C57BL/6 * V stock

Genotype: Lep^ob/Lep^ob
involves: C57BL/6J

Genotype: Lep^ob/Lep^ob
FVB.Cg-Lep^ob/Chua

Genotype: Lep^ob/Lep^ob
involves: C57BL/6

Genotype: Lep^ob/Lep^ob
B6.Cg-Lep^ob/JBomTac

Genotype: Lep^ob/Lep^ob
D2.Cg-Lep^ob/Chua

Genotype: Lep^ob/Lep^ob
BKS.Cg-Lep^ob/J

Additional - Lep^ob related