Overview

Also Known As: DBA/2J Akita, DBA-Akita, DBA/2-Akita

Heterozygous Ins2^Akita mice develop insulin dependent diabetes, including hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, which is more severe in the males than females. Obesity and insulitis do not accompany diabetes. This strain may be useful for studying diabetic complications such as nephropathy.

Donating Investigator

Dr. Matthew Breyer, Eli Lilly and Company

Genetic overview

Genetic Background	Generation
000671 DBA/2J

Ins2^Akita

Allele Type	Gene Symbol	Gene Name
Spontaneous	Ins2	insulin II

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Research Applications

Diabetes and Obesity Research
Cell Biology Research
Developmental Biology Research
Internal/Organ Research
Endocrine Deficiency Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

DBA/2J mice heterozygous for the Akita spontaneous mutation are viable and fertile. The donating investigator reports that the symptoms in heterozygous mutant mice are more severe and progressive in the males than in the females and include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. Obesity and insulitis do not accompany diabetes. Litter sizes range from 2-8 pups. Heterozygous Akita males develop albuminuria at two months of age. The albuminuria is progressive such that by 6 months of age albumin/creatine levels are approximately 600ug/mg. Additionally, it has been reported that DBA/2J heterozygous mutant mice develop diabetic nephropathy.

Although not studied in the DBA/2J heterozygotes, C57BL/6 heterozygous mutant mice exhibit gait disturbance and decreased sensory nerve conduction velocity, but do not exhibit learning or memory deficits (Choeiri C et al., 2005). Progressive retinal abnormalities begin as early as 12 weeks after the onset of hyperglycemia, and complications include increased vascular permeability, alterations in the morphology of astrocytes and microglia, increased apoptosis and thinning of the inner layers of the retina. (Barber AJ, et al., 2005) The mean lifespan of diabetic male mice on the C57BL/NJcl background (305 days) was significantly shorter than that of nondiabetic males in another colony of the same strain (690 days). Mortality rates of diabetic and nondiabetic female mice of this strain did not differ significantly.

Islets from Akita mutant mice are depleted of beta cells and the remaining beta cells release very little mature insulin. This, and the finding that mutant mice respond to exogenously administered insulin, indicate that Ins2^Akita mice will serve as an excellent substitute for mice made insulin dependent diabetic by treatment with alloxan or streptozotocin. Heterozygous Akita mice are also ideally suited to allogeneic or xenogeneic islet transplantation protocols because treating the mice diabetogen is not required to induce the hyperglycemic state. Homozygotes untreated with insulin rarely survive beyond 12 weeks of age.

This strain may be useful as a model for insulin-dependent diabetes, and in studies involving diabetic nephropathy.

Metabolic phenotype data may be found on the Diabetic Complications Consortium (DiaComp) website.

Development

Ins2^Akita is a dominant, spontaneous, point mutation, that introduces a Cys to Tyr substitution at the seventh amino acid in the A chain of mature insulin (amino acid 96 in the preproinsulin II sequence), and results in a major conformational change in the insulin 2 molecule. The Ins2^Akita spontaneous mutation on the C57BL/6 background (Stock No. 003548) was backcrossed to DBA/2J for 12 generations. In 2007, the Type 1 Diabetes Resource mated the strain to DBA/2J for 1 generation prior to initiating sibling matings.

Control Suggestions

Wild-type from the colony
000671 DBA/2J

Additional Information

Considerations for Choosing Controls

Selected References

Gurley SB; Mach CL; Stegbauer J; Yang J; Snow KP; Hu A; Meyer TW; Coffman TM. 2010. Influence of genetic background on albuminuria and kidney injury in Ins2(+/C96Y) (Akita) mice. Am J Physiol Renal Physiol 298(3):F788-95PubMed: 20042456 MGI: J:157873

View All References

Genetics

Ins2^Akita

Allele Symbol: Ins2^Akita

Allele Name	Akita
Allele Type	Spontaneous
Allele Synonym(s)	Akita; Ins2^Akita
Gene Symbol and Name	Ins2, insulin II
Gene Synonym(s)	expressed sequence AA986540; Mody; Ins-2; Mody4; Mody; MODY10; AA986540; maturity onset diabetes of the young 4; ILPR; Ins-2; InsII; IRDN; maturity onset diabetes of the young; Mody4; IDDM1; IDDM2; IDDM; CP-II
Strain of Origin	C57BL/6NSlc
Chromosome	7
Molecular Note	In the mutant allele a transition from G to A at nucleotide 1907 disrupted an Fnu4HI site in exon 3. This mutation changed the seventh amino acid in the A chain of mature insulin, Cys96 (TGC), to Tyr (TAC). The authors predict that the transition would disrupt a disulfide bond between the A and the B chains and would likely induce a major conformational change in insulin 2 molecules. RT-PCR studies suggest that both normal and mutant Ins2 alleles are transcribed similarly in pancreatic islets of heterozygous mice, although immunofluorescence and immunoblot analyses of heterozygous islets detected reduced levels of insulin and proinsulin.

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

permanent neonatal diabetes mellitus

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

maturity-onset diabetes of the young

Research Areas By Genotype

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

Genotype: Ins2^Akita related

Diabetes and Obesity Research
- Type 1 Diabetes (IDDM)
  - MODY, mature onset diabetes of the young
- Impaired Insulin Processing
- Islet Transplantation Studies
- Hyperglycemia
- Hypoinsulinemia
- Insulin Receptors and Growth Factors
Cell Biology Research
- Protein Processing
Endocrine Deficiency Research
- Pancreas Defects

Developmental Biology Research
- Internal/Organ Defects
  - kidney
Internal/Organ Research
- Kidney Defects

Mammalian Phenotype Terms by Genotype

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

Genotype: Ins2^Akita/Ins2⁺
C57BL/6-Ins2

adipose tissue phenotype

decreased subcutaneous adipose tissue amount
- mutants have almost no subcutaneous fat

cellular phenotype

abnormal mitochondrion morphology
- mutant mice show greater mitochondrial damage than wild-type or Bdkrb2-deficient mice at 12 months of age

endocrine/exocrine gland phenotype

abnormal Leydig cell morphology
- mutant males display some pigmented vacuoles in Leydig cells in the testes, but to a lesser extent than in double mutant males at 12 months of age

abnormal pancreatic beta cell morphology
- beta cells have increased amounts of endoplasmic reticulum and Golgi complexes, more and enlarged mitochondria, and partial degranulation
- density of beta cells is decreased at 14 days of age

decreased insulin secretion
- hyposecretion of insulin is seen; however, islet area is not reduced
- the pancreatic ratio of insulin to glucagon is decreased to 0.42 and 0.54 at birth and 14 days of age, respectively compared to 1.17 and 1.11 in wild-type mice

degranulated pancreatic beta cells
- partial degranulation

growth/size/body region phenotype

decreased body weight
- 7-8 week old males exhibit decreased weight as compared to controls (24g v. 26g)

postnatal growth retardation
- weight gain is normal through 18 weeks of age but then no further weight gain is seen and by 30 weeks weight loss is observed

homeostasis/metabolism phenotype

decreased circulating insulin level
- insulin levels are decreased in the blood and pancreas

decreased insulin secretion
- hyposecretion of insulin is seen; however, islet area is not reduced
- the pancreatic ratio of insulin to glucagon is decreased to 0.42 and 0.54 at birth and 14 days of age, respectively compared to 1.17 and 1.11 in wild-type mice

hyperglycemia
- blood glucose in fed 7-8 week old males measures 544+/-11 mg/dl
- develops soon after weaning and is more severe in males

impaired glucose tolerance

behavior/neurological phenotype

akinesia
- 7-8 week old males exhibit increased immobility time as measured in open field test

hypoactivity
- 7-8 week old males exhibit decreased locomotor activity as measured in open field test
- number of total entries in elevated plus maze is decreased in 7-8 week old males as compared to controls

increased anxiety-related response
- 7-8 week old males exhibit greater anxiety behavior in elevated plus maze
- total number and total time of entries in the open arms is significantly decreased as compared to controls

increased fluid intake
- 7-8 week old males consume 7 fold more water as compared to controls (33.28 ml/day v. 4.68 ml/day)

polydipsia
- develops soon after weaning and is more severe in males

polyphagia
- 7-8 week old males consume 2 fold more food as compared to controls (8.16 g/day v. 4.48 g/day)

integument phenotype

decreased subcutaneous adipose tissue amount
- mutants have almost no subcutaneous fat

mortality/aging

premature death
- 50% survival time in males is reduced to 305 days but survival time is not reduced for females through 370 days of age
- mice have much shorter lifespan than wild-type; 909 days (wt) vs 373 days (mutant)

renal/urinary system phenotype

hydronephrosis
- seen in all diabetic males but only 5 of 20 diabetic females

polyuria
- develops soon after weaning and is more severe in males

reproductive system phenotype

abnormal Leydig cell morphology
- mutant males display some pigmented vacuoles in Leydig cells in the testes, but to a lesser extent than in double mutant males at 12 months of age

skeleton phenotype

decreased bone mineral density
- mutants have significantly reduced bone density compared to wild-type or Bdkrb2-deficient mice

kyphosis
- diabetic mice display kyphosis but to a lesser extent than double mutant mice

Genotype: Ins2^Akita/Ins2⁺
involves: C3H * C57BL/6NJcl * C57BL/6NSlc

homeostasis/metabolism phenotype

hyperglycemia
- progressive increase in morning blood glucose level is seen

impaired glucose tolerance

Genotype: Ins2^Akita/Ins2^Akita
C57BL/6-Ins2

endocrine/exocrine gland phenotype

abnormal pancreatic alpha cell morphology
- alpha cell density is markedly increased

abnormal pancreatic beta cell morphology
- beta cell granules are fewer in number and smaller and mitochondrial swelling and an increase in endoplasmic reticulum are seen at 2 weeks of age
- density of beta cells is decreased within 24 hours of birth and at 2 weeks of age

decreased insulin secretion
- the pancreatic ratio of insulin to glucagon is decreased to 0.21 and 0.01 at birth and 14 days of age, respectively, compared to 1.17 and 1.11 in wild-type mice

small pancreatic islets
- islet area is reduced

homeostasis/metabolism phenotype

decreased insulin secretion
- the pancreatic ratio of insulin to glucagon is decreased to 0.21 and 0.01 at birth and 14 days of age, respectively, compared to 1.17 and 1.11 in wild-type mice

hyperglycemia
- blood glucose levels are slightly higher at 1 day of age and much higher at 14 days of age with no gender differences seen

mortality/aging

postnatal lethality

Genotype: Ins2^Akita/Ins2⁺
C57BL/6-Ins2/J

cardiovascular system phenotype

abnormal retinal vasculature morphology
- after 31-36 weeks of hyperglycemia, a modest increase in the number of acellular capillaries is seen in the retina

increased vascular permeability
- vascular permeability is increased in the retina

immune system phenotype

abnormal microglial cell morphology
- after 31-36 weeks of hyperglycemia, retinal microglia have a reactive morphology

abnormal response to transplant
- islets initially become euglycemic but revert to hyperglycemia because of rejection of the graft
- hyperglycemic male mice transplanted with pancreatic islets from wild-type B6 males become euglycemic in one week after transplant and remain euglycemic until removal of the graft (8 weeks); male mice receiving an allogeneic transplant of BALB/c wild-type islets initially become euglycemic but revert to hyperglycemia because of rejection of the graft

increased leukocyte cell number
- after 31-36 weeks of hyperglycemia, the number of leukocytes per retina is increased

nervous system phenotype

abnormal astrocyte morphology
- after 31-36 weeks of hyperglycemia, astrocytes close to large caliber superficial blood vessels in the retina have short projections that do not conjoin with the vessel

abnormal microglial cell morphology
- after 31-36 weeks of hyperglycemia, retinal microglia have a reactive morphology

vision/eye phenotype

abnormal retinal ganglion layer morphology
- after 22 weeks of hyperglycemia, the number of nuclei in the retinal ganglion cell layer is reduced by 23.4%

abnormal retinal neuronal layer morphology
- after 22 weeks of hyperglycemia, in the peripheral regions the inner nuclear layer and inner plexiform layer thickness are reduced by 15.6% and 27%, respectively, and in the central region the thickness of the inner plexiform layer is reduced by 16.7%

abnormal retinal vasculature morphology
- after 31-36 weeks of hyperglycemia, a modest increase in the number of acellular capillaries is seen in the retina

increased retinal apoptosis
- after 31-36 weeks of hyperglycemia, significantly more caspase-3 positive cells are seen

cellular phenotype

increased retinal apoptosis
- after 31-36 weeks of hyperglycemia, significantly more caspase-3 positive cells are seen

growth/size/body region phenotype

decreased body weight
- at death heterozygous males weigh significantly less than wild-type males

hematopoietic system phenotype

abnormal microglial cell morphology
- after 31-36 weeks of hyperglycemia, retinal microglia have a reactive morphology

increased leukocyte cell number
- after 31-36 weeks of hyperglycemia, the number of leukocytes per retina is increased

homeostasis/metabolism phenotype

hyperglycemia
- heterozygous males and females are hyperglycemic by 6 weeks of age (plasma glucose - 325 mg/dL); at 12 and 18 weeks of age, plasma glucose levels in males have appproximately doubled (645 mg/dL and 666 mg/dL) while levels in female mutants have increased much less (341 and 298 mg/dL respectively)
- much less (341 and 298 mg/dL respectively)

increased insulin sensitivity
- diabetic males that are hyperglycemic (plasma glucose - ~660 mg/dL) at 12 weeks show a return to euglycemia one hour after receiving 1 unit of insulin, demonstrating insulin sensitivity

Genotype: Ins2^Akita/Ins2^Akita
C57BL/6-Ins2/J

homeostasis/metabolism phenotype

hyperglycemia
- homozygous mice rapidly become hyperglycemic

mortality/aging

premature death
- untreated homozygous mice rarely survive past 12 weeks of age, with death resulting from extreme hyperglycemia;

Genotype: Ins2^Akita/Ins2^Akita
involves: C57BL/6NSlc

cardiovascular system phenotype

hematoma
- greater hematoma expansion induced by autologous blood injection in diabetic mice

cellular phenotype

increased pancreatic islet cell apoptosis
- expression of apoptosis markers in the pancreas islet is increased compared to in wild-type mice

endocrine/exocrine gland phenotype

abnormal pancreas physiology
- expression of a proliferation marker in the pancreas islet is decreased compared to in wild-type mice

decreased insulin secretion
- pancreas insulin levels are lower than in Cebpb^tm1.1Maka homozygotes

decreased pancreatic beta cell mass
- in 50% of mice at 8 weeks

increased pancreatic islet cell apoptosis
- expression of apoptosis markers in the pancreas islet is increased compared to in wild-type mice

homeostasis/metabolism phenotype

decreased circulating insulin level

decreased insulin secretion
- pancreas insulin levels are lower than in Cebpb^tm1.1Maka homozygotes

hyperglycemia

Genotype: Ins2^Akita/?
involves: C57BL/6NSlc

adipose tissue phenotype

decreased adipocyte glucose uptake
- insulin-stimulated glucose uptake in brown adipose tissue is reduced during hyperinsulinemic-euglycemic clamps

decreased body fat mass
- whole body fat mass is reduced at 8 and 3 weeks of age, however whole body lean mass is no different from wild-type

increased adipocyte glucose uptake
- insulin-stimulated glucose uptake in white adipose tissue is increased more than 3-fold during hyperinsulinemic-euglycemic clamps

cellular phenotype

decreased adipocyte glucose uptake
- insulin-stimulated glucose uptake in brown adipose tissue is reduced during hyperinsulinemic-euglycemic clamps

decreased muscle cell glucose uptake
- chronic treatment with phloridzin to chronically lower circulating glucose levels improves muscle glucose metabolism
- during hyperinsulinemic-euglycemic clamps, skeletal muscle glucose uptake is reduced by about 30%

increased adipocyte glucose uptake
- insulin-stimulated glucose uptake in white adipose tissue is increased more than 3-fold during hyperinsulinemic-euglycemic clamps

growth/size/body region phenotype

decreased body fat mass
- whole body fat mass is reduced at 8 and 3 weeks of age, however whole body lean mass is no different from wild-type

decreased body weight

homeostasis/metabolism phenotype

abnormal glucose homeostasis
- basal hepatic glucose production is increased
- during hyperinsulinemic-euglycemic clamps, insulin-stimulated whole body glycolysis and glycogen plus lipid synthesis are reduced by 40-50%
- during hyperinsulinemic-euglycemic clamps, mutants show a 40% reduction in insulin-stimulated whole body glucose turnover
- hepatic glucose production remains elevated during the insulin clamp unlike in wild-type mice which show a decrease

decreased circulating insulin level
- fed insulin levels are reduced

decreased circulating triglyceride level
- following an overnight fast and phloridzin treatment to lower plasma glucose levels, basal plasma triglyceride levels are reduced by 40%
- however, the insulin clamp has no effect on plasma triglyceride levels in mutants compared to wild-type mice in which there is a 50% reduction

decreased liver triglyceride level
- intrahepatic triglyceride levels are reduced during hyperinsulinemic-euglycemic clamps

decreased respiratory quotient
- respiratory exchange ratio is reduced, indicating increased lipid oxidation

decreased triglyceride level
- during hyperinsulinemic-euglycemic clamps, intramuscular triglyceride levels are reduced by almost 90%

hyperglycemia
- mutants develop overnight-fasted hyperglycemia

increased carbon dioxide production
- both rate of oxygen consumption and carbon dioxide production are increased by about 40%

increased energy expenditure
- mutants show increased energy expenditure during a 24 hour cycle

increased oxygen consumption
- both rate of oxygen consumption and carbon dioxide production are increased by about 40%

insulin resistance
- chronic treatment with phloridzin to chronically lower circulating glucose levels normalizes peripheral insulin action but does not normalize hepatic insulin action
- nonobese mutants develop insulin resistance in skeletal muscle, liver, and brown adipose tissue, as indicated by an approximate 80% reduction in glucose infusion rate during hyperinsulinemic-euglycemic clamps

liver/biliary system phenotype

decreased liver triglyceride level
- intrahepatic triglyceride levels are reduced during hyperinsulinemic-euglycemic clamps

muscle phenotype

abnormal cardiac muscle contractility
- chronic treatment with phloridzin to chronically lower circulating glucose levels normalizes cardiac function
- ventricular fractional shortening and ejection fraction are altered in mutants

decreased muscle cell glucose uptake
- chronic treatment with phloridzin to chronically lower circulating glucose levels improves muscle glucose metabolism
- during hyperinsulinemic-euglycemic clamps, skeletal muscle glucose uptake is reduced by about 30%

heart left ventricle hypertrophy
- ventricular hypertrophy

behavior/neurological phenotype

hypoactivity
- mutants are less active during a 24 hour cycle

increased food intake
- daily food intake is increased twofold

cardiovascular system phenotype

abnormal cardiac muscle contractility
- chronic treatment with phloridzin to chronically lower circulating glucose levels normalizes cardiac function
- ventricular fractional shortening and ejection fraction are altered in mutants

abnormal heart left ventricle morphology
- left ventricular posterior wall thickness is increased

abnormal heart morphology
- cardiac remodeling

heart left ventricle hypertrophy
- ventricular hypertrophy

thick interventricular septum

Genotype: Ins2^Akita/Ins2^Akita
C.B6N-Ins2

cardiovascular system phenotype

abnormal glomerular capillary morphology
- mice show a decrease in CD31 positive structures in the glomeruli, indicating collapse of the glomerular tufts

growth/size/body region phenotype

decreased body weight
- reduced body weight at 4 and 6 months of age

homeostasis/metabolism phenotype

albuminuria
- 3-fold increase in albumin-to-creatine ratio at 4 months of age; albuminuria persists in mutants at 6 months of age

hyperglycemia

mortality/aging

premature death
- approximately 20% of mutants fail to thrive and are sacrificed at 6 months of age

renal/urinary system phenotype

abnormal glomerular capillary morphology
- mice show a decrease in CD31 positive structures in the glomeruli, indicating collapse of the glomerular tufts

abnormal kidney interstitium morphology
- Normal - however, tubulointerstitial fibrosis is not observed
- small increase in collagen I in the tubulointerstitial compartment of the kidney

albuminuria
- 3-fold increase in albumin-to-creatine ratio at 4 months of age; albuminuria persists in mutants at 6 months of age

expanded mesangial matrix
- mesangial matrix expansion is seen at 4 months of age and is more pronounced than in heterozygous mice

glomerulosclerosis
- same degree of glomerular injury as in heterozygotes at 6 months of age

increased renal glomerular filtration rate
- glomerular filtration rate is increased at 4 months of age but decreased by 6 months of age to normal levels

increased renal glomerulus basement membrane thickness

renal glomerular protein deposits
- increase in glomerular collagen IV deposition at 6 months of age

Genotype: Ins2^Akita/Ins2⁺
C.B6N-Ins2

homeostasis/metabolism phenotype

albuminuria
- 3-fold increase in albumin-to-creatine ratio at 4 months of age, however albuminuria does not persist at 6 months of age

renal/urinary system phenotype

albuminuria
- 3-fold increase in albumin-to-creatine ratio at 4 months of age, however albuminuria does not persist at 6 months of age

expanded mesangial matrix
- mesangial matrix expansion is seen at 4 months of age

glomerulosclerosis
- same degree of glomerular injury as in homozygotes at 6 months of age

increased renal glomerular filtration rate
- glomerular filtration rate is increased at 6 months of age

Genotype: Ins2^Akita/Ins2⁺
involves: C57BL/6NSlc

behavior/neurological phenotype

increased food intake

endocrine/exocrine gland phenotype

abnormal pancreatic islet morphology
- beta cells contain a small number of secretory granules, a tubulovesicular structure comprised of enlarged endoplasmic reticulum, and swelling or disruption of mitochondria

decreased insulin secretion
- decreased total pancreatic insulin and prolinsulin content

growth/size/body region phenotype

decreased body weight

homeostasis/metabolism phenotype

decreased circulating leptin level

decreased insulin secretion
- decreased total pancreatic insulin and prolinsulin content

increased circulating glucose level

mammalian phenotype

homeostasis/metabolism phenotype
- Normal - mice exhibit normal insulin sensitivity

References

Gurley SB; Mach CL; Stegbauer J; Yang J; Snow KP; Hu A; Meyer TW; Coffman TM. 2010. Influence of genetic background on albuminuria and kidney injury in Ins2(+/C96Y) (Akita) mice. Am J Physiol Renal Physiol 298(3):F788-95PubMed: 20042456 MGI: J:157873

Additional - Ins2^Akita related

Technical Support

Contact Technical Support

Genotyping Protocols
- Restriction Enzyme Digest: Ins2^Akita
- End Point Analysis: Ins2^Akita
- Genotyping resources and troubleshooting
Mating System
- +/+ sibling x Heterozygote
Citation
When using the DBA/2-Akita mouse strain in a publication, please cite the originating article(s) and include JAX stock #007562 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

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

Pricing & Availability

Cryo Recovery

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Genotype

Price

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Cryorecovery - Pricing

Service	Genotype	Price
	Heterozygous or Wild-type for Ins2<Akita>

We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

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Also Known As: DBA/2J Akita, DBA-Akita, DBA/2-Akita

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Ins2Akita

Allele Symbol: Ins2Akita

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Genotype

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

Genotype: Ins2Akita related

Mammalian Phenotype Terms by Genotype

Genotype: Ins2Akita/Ins2+C57BL/6-Ins2

adipose tissue phenotype

cellular phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

behavior/neurological phenotype

integument phenotype

mortality/aging

renal/urinary system phenotype

reproductive system phenotype

skeleton phenotype

Genotype: Ins2Akita/Ins2+involves: C3H * C57BL/6NJcl * C57BL/6NSlc

homeostasis/metabolism phenotype

Genotype: Ins2Akita/Ins2AkitaC57BL/6-Ins2

endocrine/exocrine gland phenotype

homeostasis/metabolism phenotype

mortality/aging

Genotype: Ins2Akita/Ins2+C57BL/6-Ins2/J

cardiovascular system phenotype

immune system phenotype

nervous system phenotype

vision/eye phenotype

cellular phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

Genotype: Ins2Akita/Ins2AkitaC57BL/6-Ins2/J

homeostasis/metabolism phenotype

mortality/aging

Genotype: Ins2Akita/Ins2Akitainvolves: C57BL/6NSlc

cardiovascular system phenotype

cellular phenotype

endocrine/exocrine gland phenotype

homeostasis/metabolism phenotype

Genotype: Ins2Akita/?involves: C57BL/6NSlc

adipose tissue phenotype

cellular phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

liver/biliary system phenotype

muscle phenotype

behavior/neurological phenotype

cardiovascular system phenotype

Genotype: Ins2Akita/Ins2AkitaC.B6N-Ins2

cardiovascular system phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

mortality/aging

renal/urinary system phenotype

Genotype: Ins2Akita/Ins2+C.B6N-Ins2

homeostasis/metabolism phenotype

renal/urinary system phenotype

Genotype: Ins2Akita/Ins2+involves: C57BL/6NSlc

behavior/neurological phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

mammalian phenotype

References

Ins2^Akita

Allele Symbol: Ins2^Akita

Genotype: Ins2^Akita related

Genotype: Ins2^Akita/Ins2⁺
C57BL/6-Ins2

Genotype: Ins2^Akita/Ins2⁺
involves: C3H * C57BL/6NJcl * C57BL/6NSlc

Genotype: Ins2^Akita/Ins2^Akita
C57BL/6-Ins2

Genotype: Ins2^Akita/Ins2⁺
C57BL/6-Ins2/J

Genotype: Ins2^Akita/Ins2^Akita
C57BL/6-Ins2/J

Genotype: Ins2^Akita/Ins2^Akita
involves: C57BL/6NSlc

Genotype: Ins2^Akita/?
involves: C57BL/6NSlc

Genotype: Ins2^Akita/Ins2^Akita
C.B6N-Ins2

Genotype: Ins2^Akita/Ins2⁺
C.B6N-Ins2

Genotype: Ins2^Akita/Ins2⁺
involves: C57BL/6NSlc

Additional - Ins2^Akita related