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Featured JAX Mice Models of Type 2 Diabetes & Obesity

Name & Stock Number B6.Cg-Lepob/J
(000632)		 B6.BKS(D)-Leprdb/J
(000697)		 BKS.Cg-Dock7m +/+ Leprdb/J
(000642)
Common Name B6 ob B6 db BKS db
Benefits
  • Hyperphagic, becoming obese by four weeks of age
  • Glucose intolerance with transient hyperglycemia (subsiding by 14-16 weeks) followed by hyperinsulinemia
  • Pancreatic beta cell hypertrophy without islet atrophy
  • Increased circulating total cholesterol (including HDL, LDL and VLDL)
  • Hypometabolic, hypothermic, and abnormally high levels of pituitary and adrenal hormones
  • Hyperphagic, becoming obese by four weeks of age
  • Glucose intolerance with transient hyperglycemia (subsiding by 14-16 weeks) followed by hyperinsulinemia
  • Pancreatic beta cell hypertrophy without islet atrophy
  • Increased circulating total cholesterol (including HDL, LDL and VLDL)
  • Hypometabolic, hypothermic, and abnormally high levels of pituitary and adrenal hormones
  • Hyperphagic, becoming obese by four weeks of age
  • Glucose intolerance with prolonged hyperglycemia by 8 weeks of age and transient hyperinsulinemia
  • Polydipsic, polyuric, increased gluconeogenic enzyme activity and increased metabolic efficiency
Considerations
  • Infertility (homozygous females); subfertility (homozygous males)
  • Impaired wound healing
  • Infertility (homozygous females); subfertility (homozygous males)
  • Impaired wound healing
  • Severe islet atrophy causing hypoinsulinemia and death by 10 months of age
  • Peripheral neuropathy, nephropathy, myocardial disease, and impaired wound healing
  • Infertility (homozygous females); subfertility (homozygous males)
Phenotyping Details Phenotype information for 000632 Phenotype information for 000697 Phenotype information for 000642
References Genuth et al. 1971, Dubuc 1976; Dong et al. 2006 Genuth et al. 1971, Dubuc 1976; Dong et al. 2006 Hummel et al. 1966; Like et al. 1970; Norido et al. 1984, Wendt et al. 2003, Giacomelli et al. 1979, Werner et al. 1994
Name & Stock Number C57BL/6J Diet-Induced Obesity
(380050)		 NONcNZO10/LtJ
(004456)		 TALLYHO/JngJ
(005314)
Common Name B6 DIO RCS-10 TH
Benefits
  • Diet-induced obesity when fed a 60 kcal% high fat diet
  • Pre-diabetic fed blood glucose levels with glucose intolerance by 8 weeks of age
  • Improved glucose tolerance and insulin resistance when treated with Rosiglitazone
  • Pancreatic beta cell hypertrophy without islet atrophy
  • Hyperinsulinemia, hyperleptinemia, leptin resistance, and hypertension
  • Moderate diet-induced obesity without hyperphagia when fed a 27 kcal% (10-11% wt/wt) fat diet
  • Males transition from impared glucose tolerance to stable non-fasting hyperglycemia by 10 weeks of age
  • Moderately elevated plasma insulin, islets transition from hypertrophy and hyperplasia to atrophy by 24 weeks
  • Elevated leptin and triglycerides
  • Moderate obesity in both males and females
  • Males are normoglycemic at weaning, become glucose intolerant by 4 weeks, and begin developing hyperglycemia by 10-14 weeks of age
  • Males are hyperinsulinemic, exhibiting plasma insulin levels between 8-12 ng/ml by 8 weeks of age
  • Both sexes develop pancreatic islet hypertrophy and hyperplasia
  • Males have severe dyslipidemia, with elevated triglycerides, total cholesterol, HDL cholesterol, and free fatty acids
Considerations
  • Mild glomerulosclerotic changes
  • Males respond to high-dose Rosiglitazone with lower blood glucose and improved glucose tolerance (The Jackson Laboratory, unpublished)
Phenotyping Details Phenotyping and effects of rosiglitazone on DIO Mice Phenotype information for 004456 Phenotyping information and effects of rosiglitazone for 005314
References Collins et al. 2004; Petro et al. 2004; Rossmeisl et al. 2003; Van Heek et al. 1997; Surwit et al. 1995 Leiter and Reifsnyder 2004; Reifsnyder and Leiter 2002 Kim et al. 2001, 2005, 2006
Name & Stock Number KK.Cg-Ay/J
(002468)		 BTBR.Cg-Lepob/WiscJ
(004824)		 BKS.Cg-Leprdb Nos3tm1Unc/RhrsJ
(008340)
Common Name KK-Ay, KKAy BTBR obese eNOS-/- C57BLKS/Jdb
Benefits
  • Hyperphagia with moderate obesity
  • Early, severe hyperglycemia and glucose intolerance
  • Hyperinsulinemia and insulin resistance, with islet hypertrophy and hyperplasia
  • Elevated HbA1c and microalbuminuria
  • Hyperphagic, leading to significant obesity by 6 weeks of age
  • Male and female homozygotes are diabetic by 4 weeks of age
  • Severe hyperglycemia, with serum glucose levels of 400 mg/dl and HbA1c > 8 NGSP% by 8 weeks
  • Dyslipidemia, with very elevated triglycerides in males
  • Diabetic nephropathy: urine albumin:creatinine ratio increased in both sexes
  • Early hypersecretion of insulin, then islets atrophy and mice become hypoinsulinemic at > 16 weeks of age
  • Moderate systemic hypertension and rapidly progressive diabetic nephropathy
  • Hyperphagic, becoming obese by four weeks of age
  • Glucose intolerance with severe hyperglycemia by 8 weeks of age and transient hyperinsulinemia
  • Severe islet atrophy causing hypoinsulinemia and death by 10 months of age
  • Polydipsic, polyuric, increased gluconeogenic enzyme activity and increased metabolic efficiency
Considerations
  • Males develop diabetic glomerular nephritis and arteriosclerosis
  • Early glomerular nephropathy by 8 weeks and histological characteristics of advanced diabetic nephropathy by 20-22 weeks
  • Peripheral neuropathy, nephropathy, myocardial disease, and delayed wound healing
  • Infertility (homozygous females); subfertility (homozygous males)
Phenotyping Details Phenotype information for 002468 Phenotype information for 004824 Phenotype information for 008340
References Okazaki et al. 2002; Asano et al. 2004; Iwatsuka et al. 1970; (Chang AY et al. 1986. The Upjohn colony of KKAy mice: a model of obese type II diabetes. In: Diabetes 1985. Serrano-Rios M, Lefebvre PJ (eds), Elsevier. Pp.466-70) Lan et al. 2003; Clee et al. 2005; Hudkins et al. 2010 Zhao et al. 2006; Hummel et al. 1966; Like et al. 1970; Norido et al. 1984, Wendt et al. 2003, Giacomelli et al. 1979, Werner et al. 1994
Name & Stock Number MSNASH/PcoJ
(030888)
Common Name MS-NASH
Benefits
  • Has an intact leptin pathway (similar to the human disease)
  • Exhibits spontaneous obesity, dyslipidemia, rapid insulin resistance, high level of insulin secretion as hypersulinemia
  • Develops liver steatosis leading to NAFLD/NASH
  • Responds to anti-diabetic standard of care treatments e.g. Semaglutide (Ozempic®) that results in a reduction of body weight, food intake, and blood glucose levels
Considerations
  • Females do not exhibit the diabetic phenotype
References Asgharpour et al., 2016, Peterson et al., 2017
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