JAX
Mouse Strain Datasheet - 007562
D2.B6-Ins2Akita/MatbJ
Also Known As: DBA/2-Akita, DBA-Akita, DBA/2J Akita
Heterozygous Ins2Akita 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 |
N14p+N1F1N4F9
|
Ins2Akita
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Spontaneous | Ins2 | insulin II |
Research Applications
- Developmental Biology Research
- Internal/Organ Research
- Cell Biology Research
- Diabetes and Obesity Research
- Endocrine Deficiency Research
Base Price
Starting at:
| $224.00 Domestic price for female |
| $258.30 Domestic price for breeder pair |
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 Ins2Akita 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
Ins2Akita 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 Ins2Akita 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
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):F788-95. PubMed: 20042456MGI: J:157873
Ins2Akita
Allele Symbol: Ins2Akita
| Allele Name | Akita |
|---|---|
| Allele Type | Spontaneous |
| Allele Synonym(s) | Akita; AkitaIns2; Ins2C96Y; Ins2Mody; Mody; Mody4 |
| Gene Symbol and Name | Ins2, insulin II |
| Gene Synonym(s) | AA986540; CP-II; IDDM; IDDM1; IDDM2; ILPR; IRDN; Ins-2; Ins-2; InsII; MODY10; Mody; Mody; Mody4; Mody4; expressed sequence AA986540; maturity onset diabetes of the young; maturity onset diabetes of the young 4 |
| 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 Terms
Research Areas By Genotype
This mouse can be used to support research in many areas including:
- Developmental Biology Research
- Internal/Organ Defects
- kidney
- Internal/Organ Defects
- Internal/Organ Research
- Kidney Defects
Genotype: Ins2Akita related
- Cell Biology Research
- Protein Processing
- Diabetes and Obesity Research
- Hyperglycemia
- Hypoinsulinemia
- Impaired Insulin Processing
- Insulin Receptors and Growth Factors
- Islet Transplantation Studies
- Type 1 Diabetes (IDDM)
- MODY, mature onset diabetes of the young
- Endocrine Deficiency Research
- Pancreas 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: Ins2Akita/Ins2+
C.B6N-Ins2Akita
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 (MGI Ref ID J:198186)
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 (MGI Ref ID J:198186)
- expanded mesangial matrix
- mesangial matrix expansion is seen at 4 months of age (MGI Ref ID J:198186)
- glomerulosclerosis
- same degree of glomerular injury as in homozygotes at 6 months of age (MGI Ref ID J:198186)
- increased renal glomerular filtration rate
- glomerular filtration rate is increased at 6 months of age (MGI Ref ID J:198186)
Genotype: Ins2Akita/Ins2+
involves: C57BL/6NSlc
homeostasis/metabolism phenotype
- decreased circulating leptin level
- (MGI Ref ID J:200802)
- decreased insulin secretion
- decreased total pancreatic insulin and prolinsulin content (MGI Ref ID J:200802)
- homeostasis/metabolism phenotype
- mice exhibit normal insulin sensitivity (MGI Ref ID J:200802)
- increased circulating glucose level
- (MGI Ref ID J:200802)
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 (MGI Ref ID J:200802)
- decreased insulin secretion
- decreased total pancreatic insulin and prolinsulin content (MGI Ref ID J:200802)
growth/size/body region phenotype
- decreased body weight
- (MGI Ref ID J:200802)
behavior/neurological phenotype
- increased food intake
- (MGI Ref ID J:200802)
Genotype: Ins2Akita/Ins2+
C57BL/6-Ins2Akita/J
homeostasis/metabolism phenotype
- hyperglycemia
- (MGI Ref ID J:99412)
- 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) (MGI Ref ID J:76224)
- 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 (MGI Ref ID J:76224)
immune system phenotype
- abnormal microglial cell morphology
- after 31-36 weeks of hyperglycemia, retinal microglia have a reactive morphology (MGI Ref ID J:99412)
- abnormal response to transplant
- 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 islets initially become euglycemic but revert to hyperglycemia because of rejection of the graft (MGI Ref ID J:76224)
- increased leukocyte cell number
- after 31-36 weeks of hyperglycemia, the number of leukocytes per retina is increased (MGI Ref ID J:99412)
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 (MGI Ref ID J:99412)
- increased vascular permeability
- vascular permeability is increased in the retina (MGI Ref ID J:99412)
growth/size/body region phenotype
- decreased body weight
- at death heterozygous males weigh significantly less than wild-type males (MGI Ref ID J:99412)
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 (MGI Ref ID J:99412)
- abnormal microglial cell morphology
- after 31-36 weeks of hyperglycemia, retinal microglia have a reactive morphology (MGI Ref ID J:99412)
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% (MGI Ref ID J:99412)
- 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% (MGI Ref ID J:99412)
- abnormal retinal vasculature morphology
- after 31-36 weeks of hyperglycemia, a modest increase in the number of acellular capillaries is seen in the retina (MGI Ref ID J:99412)
- increased retinal apoptosis
- after 31-36 weeks of hyperglycemia, significantly more caspase-3 positive cells are seen (MGI Ref ID J:99412)
hematopoietic system phenotype
- abnormal microglial cell morphology
- after 31-36 weeks of hyperglycemia, retinal microglia have a reactive morphology (MGI Ref ID J:99412)
- increased leukocyte cell number
- after 31-36 weeks of hyperglycemia, the number of leukocytes per retina is increased (MGI Ref ID J:99412)
cellular phenotype
- increased retinal apoptosis
- after 31-36 weeks of hyperglycemia, significantly more caspase-3 positive cells are seen (MGI Ref ID J:99412)
Genotype: Ins2Akita/Ins2+
involves: C3H * C57BL/6NJcl * C57BL/6NSlc
homeostasis/metabolism phenotype
- hyperglycemia
- progressive increase in morning blood glucose level is seen (MGI Ref ID J:40063)
- impaired glucose tolerance
- (MGI Ref ID J:40063)
Genotype: Ins2Akita/Ins2+
C57BL/6-Ins2Akita
mortality/aging
- premature death
skeleton phenotype
- decreased bone mineral density
- mutants have significantly reduced bone density compared to wild-type or Bdkrb2-deficient mice (MGI Ref ID J:108948)
- kyphosis
- diabetic mice display kyphosis but to a lesser extent than double mutant mice (MGI Ref ID J:108948)
integument phenotype
- decreased subcutaneous adipose tissue amount
- mutants have almost no subcutaneous fat (MGI Ref ID J:108948)
homeostasis/metabolism phenotype
- decreased circulating insulin level
- insulin levels are decreased in the blood and pancreas (MGI Ref ID J:40063)
- decreased insulin secretion
- hyperglycemia
- impaired glucose tolerance
- (MGI Ref ID J:40063)
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 (MGI Ref ID J:108948)
- abnormal pancreatic beta cell morphology
- decreased insulin secretion
- degranulated pancreatic beta cells
- partial degranulation (MGI Ref ID J:47883)
renal/urinary system phenotype
- hydronephrosis
- seen in all diabetic males but only 5 of 20 diabetic females (MGI Ref ID J:40063)
- polyuria
- develops soon after weaning and is more severe in males (MGI Ref ID J:40063)
behavior/neurological phenotype
- akinesia
- 7-8 week old males exhibit increased immobility time as measured in open field test (MGI Ref ID J:125256)
- hypoactivity
- increased anxiety-related response
- 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) (MGI Ref ID J:125256)
- polydipsia
- develops soon after weaning and is more severe in males (MGI Ref ID J:40063)
- polyphagia
- 7-8 week old males consume 2 fold more food as compared to controls (8.16 g/day v. 4.48 g/day) (MGI Ref ID J:125256)
growth/size/body region phenotype
- decreased body weight
- 7-8 week old males exhibit decreased weight as compared to controls (24g v. 26g) (MGI Ref ID J:125256)
- 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 (MGI Ref ID J:40063)
adipose tissue phenotype
- decreased subcutaneous adipose tissue amount
- mutants have almost no subcutaneous fat (MGI Ref ID J:108948)
cellular phenotype
- abnormal mitochondrion morphology
- mutant mice show greater mitochondrial damage than wild-type or Bdkrb2-deficient mice at 12 months of age (MGI Ref ID J:108948)
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 (MGI Ref ID J:108948)
Genotype: Ins2Akita/Ins2Akita
involves: C57BL/6NSlc
endocrine/exocrine gland phenotype
- abnormal pancreas physiology
- expression of a proliferation marker in the pancreas islet is decreased compared to in wild-type mice (MGI Ref ID J:156725)
- decreased insulin secretion
- pancreas insulin levels are lower than in Cebpbtm1.1Maka homozygotes (MGI Ref ID J:156725)
- decreased pancreatic beta cell mass
- in 50% of mice at 8 weeks (MGI Ref ID J:156725)
- increased pancreatic islet cell apoptosis
- expression of apoptosis markers in the pancreas islet is increased compared to in wild-type mice (MGI Ref ID J:156725)
homeostasis/metabolism phenotype
- decreased circulating insulin level
- (MGI Ref ID J:156725)
- decreased insulin secretion
- pancreas insulin levels are lower than in Cebpbtm1.1Maka homozygotes (MGI Ref ID J:156725)
- hyperglycemia
- (MGI Ref ID J:156725)
cardiovascular system phenotype
- hematoma
- greater hematoma expansion induced by autologous blood injection in diabetic mice (MGI Ref ID J:168556)
cellular phenotype
- increased pancreatic islet cell apoptosis
- expression of apoptosis markers in the pancreas islet is increased compared to in wild-type mice (MGI Ref ID J:156725)
Genotype: Ins2Akita/Ins2Akita
C57BL/6-Ins2Akita
mortality/aging
- postnatal lethality
- (MGI Ref ID J:47883)
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 (MGI Ref ID J:47883)
- 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 (MGI Ref ID J:47883)
endocrine/exocrine gland phenotype
- abnormal pancreatic alpha cell morphology
- alpha cell density is markedly increased (MGI Ref ID J:47883)
- abnormal pancreatic beta cell morphology
- 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 (MGI Ref ID J:47883)
- small pancreatic islets
- islet area is reduced (MGI Ref ID J:47883)
Genotype: Ins2Akita/Ins2Akita
C.B6N-Ins2Akita
mortality/aging
- premature death
- approximately 20% of mutants fail to thrive and are sacrificed at 6 months of age (MGI Ref ID J:198186)
cardiovascular system phenotype
- abnormal glomerular capillary morphology
- mice show a decrease in CD31 positive structures in the glomeruli, indicating collapse of the glomerular tufts (MGI Ref ID J:198186)
growth/size/body region phenotype
- decreased body weight
- reduced body weight at 4 and 6 months of age (MGI Ref ID J:198186)
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 (MGI Ref ID J:198186)
- hyperglycemia
- (MGI Ref ID J:198186)
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 (MGI Ref ID J:198186)
- abnormal kidney interstitium morphology
- abnormal renal glomerulus morphology
- increase in glomerular collagen IV deposition at 6 months of age (MGI Ref ID J:198186)
- albuminuria
- 3-fold increase in albumin-to-creatine ratio at 4 months of age; albuminuria persists in mutants at 6 months of age (MGI Ref ID J:198186)
- expanded mesangial matrix
- mesangial matrix expansion is seen at 4 months of age and is more pronounced than in heterozygous mice (MGI Ref ID J:198186)
- glomerulosclerosis
- same degree of glomerular injury as in heterozygotes at 6 months of age (MGI Ref ID J:198186)
- 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 (MGI Ref ID J:198186)
- increased renal glomerulus basement membrane thickness
- (MGI Ref ID J:198186)
Genotype: Ins2Akita/Ins2Akita
C57BL/6-Ins2Akita/J
mortality/aging
- premature death
- untreated homozygous mice rarely survive past 12 weeks of age, with death resulting from extreme hyperglycemia; (MGI Ref ID J:76224)
homeostasis/metabolism phenotype
- hyperglycemia
- homozygous mice rapidly become hyperglycemic (MGI Ref ID J:76224)
Genotype: Ins2Akita/?
involves: C57BL/6NSlc
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 (MGI Ref ID J:130021)
- decreased body weight
- (MGI Ref ID J:130021)
adipose tissue phenotype
- decreased adipocyte glucose uptake
- insulin-stimulated glucose uptake in brown adipose tissue is reduced during hyperinsulinemic-euglycemic clamps (MGI Ref ID J:130021)
- 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 (MGI Ref ID J:130021)
- increased adipocyte glucose uptake
- insulin-stimulated glucose uptake in white adipose tissue is increased more than 3-fold during hyperinsulinemic-euglycemic clamps (MGI Ref ID J:130021)
behavior/neurological phenotype
- hypoactivity
- mutants are less active during a 24 hour cycle (MGI Ref ID J:130021)
- increased food intake
- daily food intake is increased twofold (MGI Ref ID J:130021)
homeostasis/metabolism phenotype
- abnormal glucose homeostasis
- basal hepatic glucose production is increased (MGI Ref ID J:130021)
- during hyperinsulinemic-euglycemic clamps, insulin-stimulated whole body glycolysis and glycogen plus lipid synthesis are reduced by 40-50% (MGI Ref ID J:130021)
- during hyperinsulinemic-euglycemic clamps, mutants show a 40% reduction in insulin-stimulated whole body glucose turnover (MGI Ref ID J:130021)
- hepatic glucose production remains elevated during the insulin clamp unlike in wild-type mice which show a decrease (MGI Ref ID J:130021)
- decreased circulating insulin level
- fed insulin levels are reduced (MGI Ref ID J:130021)
- decreased circulating triglyceride level
- following an overnight fast and phloridzin treatment to lower plasma glucose levels, basal plasma triglyceride levels are reduced by 40% (MGI Ref ID J:130021)
- 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 (MGI Ref ID J:130021)
- decreased liver triglyceride level
- intrahepatic triglyceride levels are reduced during hyperinsulinemic-euglycemic clamps (MGI Ref ID J:130021)
- decreased respiratory quotient
- respiratory exchange ratio is reduced, indicating increased lipid oxidation (MGI Ref ID J:130021)
- decreased triglyceride level
- during hyperinsulinemic-euglycemic clamps, intramuscular triglyceride levels are reduced by almost 90% (MGI Ref ID J:130021)
- hyperglycemia
- mutants develop overnight-fasted hyperglycemia (MGI Ref ID J:130021)
- increased carbon dioxide production
- both rate of oxygen consumption and carbon dioxide production are increased by about 40% (MGI Ref ID J:130021)
- increased energy expenditure
- mutants show increased energy expenditure during a 24 hour cycle (MGI Ref ID J:130021)
- increased oxygen consumption
- both rate of oxygen consumption and carbon dioxide production are increased by about 40% (MGI Ref ID J:130021)
- insulin resistance
- chronic treatment with phloridzin to chronically lower circulating glucose levels normalizes peripheral insulin action but does not normalize hepatic insulin action (MGI Ref ID J:130021)
- 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 (MGI Ref ID J:130021)
cardiovascular system phenotype
- abnormal cardiac muscle contractility
- abnormal heart left ventricle morphology
- left ventricular posterior wall thickness is increased (MGI Ref ID J:130021)
- abnormal heart morphology
- cardiac remodeling (MGI Ref ID J:130021)
- heart left ventricle hypertrophy
- ventricular hypertrophy (MGI Ref ID J:130021)
- thick interventricular septum
- (MGI Ref ID J:130021)
liver/biliary system phenotype
- decreased liver triglyceride level
- intrahepatic triglyceride levels are reduced during hyperinsulinemic-euglycemic clamps (MGI Ref ID J:130021)
muscle phenotype
- abnormal cardiac muscle contractility
- decreased muscle cell glucose uptake
cellular phenotype
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):F788-95. PubMed: 20042456MGI: J:157873
Additional - Ins2Akita related
- Abdo S; Shi Y; Otoukesh A; Ghosh A; Lo CS; Chenier I; Filep JG; Ingelfinger JR; Zhang SL; Chan JS. 2014. Catalase overexpression prevents nuclear factor erythroid 2-related factor 2 stimulation of renal angiotensinogen gene expression, hypertension, and kidney injury in diabetic mice. Diabetes 63(10):3483-96. PubMed: 24812425MGI: J:229839
- Abudukadier A; Fujita Y; Obara A; Ohashi A; Fukushima T; Sato Y; Ogura M; Nakamura Y; Fujimoto S; Hosokawa M; Hasegawa H; Inagaki N. 2013. Tetrahydrobiopterin has a glucose-lowering effect by suppressing hepatic gluconeogenesis in an endothelial nitric oxide synthase-dependent manner in diabetic mice. Diabetes 62(9):3033-43. PubMed: 23649519MGI: J:208962
- Aghdam SY; Gurel Z; Ghaffarieh A; Sorenson CM; Sheibani N. 2013. High glucose and diabetes modulate cellular proteasome function: Implications in the pathogenesis of diabetes complications. Biochem Biophys Res Commun 432(2):339-44. PubMed: 23391566MGI: J:198848
- Akimov NP; Renteria RC. 2012. Spatial frequency threshold and contrast sensitivity of an optomotor behavior are impaired in the Ins2Akita mouse model of diabetes. Behav Brain Res 226(2):601-5. PubMed: 21963766MGI: J:180197
- Asakawa A; Toyoshima M; Inoue K; Koizumi A. 2007. Ins2Akita mice exhibit hyperphagia and anxiety behavior via the melanocortin system. Int J Mol Med 19(4):649-52. PubMed: 17334640MGI: J:125256
- Awad AS; Kinsey GR; Khutsishvili K; Gao T; Bolton WK; Okusa MD. 2011. Monocyte/macrophage chemokine receptor CCR2 mediates diabetic renal injury. Am J Physiol Renal Physiol 301(6):F1358-66. PubMed: 21880831MGI: J:180042
- Bachar-Wikstrom E; Wikstrom JD; Ariav Y; Tirosh B; Kaiser N; Cerasi E; Leibowitz G. 2013. Stimulation of autophagy improves endoplasmic reticulum stress-induced diabetes. Diabetes 62(4):1227-37. PubMed: 23274896MGI: J:208584
- Barber AJ; Antonetti DA; Kern TS; Reiter CE; Soans RS; Krady JK; Levison SW; Gardner TW; Bronson SK. 2005. The Ins2Akita mouse as a model of early retinal complications in diabetes. Invest Ophthalmol Vis Sci 46(6):2210-8. PubMed: 15914643MGI: J:99412
- Basu R; Lee J; Wang Z; Patel VB; Fan D; Das SK; Liu GC; John R; Scholey JW; Oudit GY; Kassiri Z. 2012. Loss of TIMP3 selectively exacerbates diabetic nephropathy. Am J Physiol Renal Physiol 303(9):F1341-52. PubMed: 22896043MGI: J:189948
- Basu R; Oudit GY; Wang X; Zhang L; Ussher JR; Lopaschuk GD; Kassiri Z. 2009. Type 1 diabetic cardiomyopathy in the Akita (Ins2WT/C96Y) mouse model is characterized by lipotoxicity and diastolic dysfunction with preserved systolic function. Am J Physiol Heart Circ Physiol 297(6):H2096-108. PubMed: 19801494MGI: J:158228
- Blum B; Roose AN; Barrandon O; Maehr R; Arvanites AC; Davidow LS; Davis JC; Peterson QP; Rubin LL; Melton DA. 2014. Reversal of beta cell de-differentiation by a small molecule inhibitor of the TGFbeta pathway. Elife 3:e02809. PubMed: 25233132MGI: J:218054
- Bostrom KI; Jumabay M; Matveyenko A; Nicholas SB; Yao Y. 2011. Activation of vascular bone morphogenetic protein signaling in diabetes mellitus. Circ Res 108(4):446-57. PubMed: 21193740MGI: J:183498
- Bugger H; Boudina S; Hu XX; Tuinei J; Zaha VG; Theobald HA; Yun UJ; McQueen AP; Wayment B; Litwin SE; Abel ED. 2008. Type 1 diabetic akita mouse hearts are insulin sensitive but manifest structurally abnormal mitochondria that remain coupled despite increased uncoupling protein 3. Diabetes 57(11):2924-32. PubMed: 18678617MGI: J:142159
- Bugger H; Chen D; Riehle C; Soto J; Theobald HA; Hu XX; Ganesan B; Weimer BC; Abel ED. 2009. Tissue-specific remodeling of the mitochondrial proteome in type 1 diabetic akita mice. Diabetes 58(9):1986-97. PubMed: 19542201MGI: J:154406
- Chacko BK; Reily C; Srivastava A; Johnson MS; Ye Y; Ulasova E; Agarwal A; Zinn KR; Murphy MP; Kalyanaraman B; Darley-Usmar V. 2010. Prevention of diabetic nephropathy in Ins2(+/)(AkitaJ) mice by the mitochondria-targeted therapy MitoQ. Biochem J 432(1):9-19. PubMed: 20825366MGI: J:166866
- Chang AS; Dale AN; Moley KH. 2005. Maternal diabetes adversely affects preovulatory oocyte maturation, development, and granulosa cell apoptosis. Endocrinology 146(5):2445-53. PubMed: 15718275MGI: J:129826
- Chang JH; Paik SY; Mao L; Eisner W; Flannery PJ; Wang L; Tang Y; Mattocks N; Hadjadj S; Goujon JM; Ruiz P; Gurley SB; Spurney RF. 2012. Diabetic kidney disease in FVB/NJ Akita mice: temporal pattern of kidney injury and urinary nephrin excretion. PLoS One 7(4):e33942. PubMed: 22496773MGI: J:187110
- Chavali V; Tyagi SC; Mishra PK. 2012. MicroRNA-133a regulates DNA methylation in diabetic cardiomyocytes. Biochem Biophys Res Commun 425(3):668-72. PubMed: 22842467MGI: J:188036
- Chen H; Li J; Jiao L; Petersen RB; Li J; Peng A; Zheng L; Huang K. 2014. Apelin inhibits the development of diabetic nephropathy by regulating histone acetylation in Akita mouse. J Physiol 592(Pt 3):505-21. PubMed: 24247978MGI: J:217958
- Chen Q; Takahashi Y; Oka K; Ma JX. 2016. Functional Differences of Very-Low-Density Lipoprotein Receptor Splice Variants in Regulating Wnt Signaling. Mol Cell Biol 36(20):2645-54. PubMed: 27528615MGI: J:236304
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