NZO mice of both sexes exhibit high birth weights and are significantly heavier at weaning age. Severe obesity (including both visceral and subcuatneous fat depots) develops even when mice are maintained on a standard diet containing 4.5% fat. Both males and females of the NZO/Hl substrain exhibit impaired glucose tolerance (IGT), but subsequent type 2 maturity onset (NIDDM) diabetes development is limited to males, with a phenotype penetrance of 50% or less. NZO/Hl mice also show anti-insulin receptor antibodies, a defect in leptin transport, and hypertension. The genetic lesion appears to be within the islets of Langerhans as transfer of pancreatic islets from normal mice returns body weights and blood glucose levels to within normal range. Ovarian granulosa cell tumors, lymphomas, duodenal, and lung tumors have also been noted to occur in NZO mice at an elevated frequency. F1 hybrids of NON/ShiLt and NZO/Hl provide a new model of obesity-induced diabetes. Male (NON/ShiLt x NZO/Hl)F1 hybrids are obese (BW = 53.5 g by 16 weeks) and almost all develop maturity onset NIDDM. F1 males on a 4% diet will develop hyperglycemia around 20 to 24 weeks of age; increasing the fat content of the diet accelerates diabetes onset to 16 to 20 weeks of age. (NZO/Hl x NON/ShiLt)F1 hybrids will develop diabetes slightly faster than their reciprocal cross due to the NZO maternal environment; however this cross is difficult to produce due to the inherently poor breeding performance of NZO/HlJ female mice. F1 females exhibit a weight gain similar to the NZO parent, and have impaired glucose tolerance but are resistant to diabetes development. Diabetes development can be accelerated to eight to 12 weeks by fostering onto an F1 dam. Reciprocal backcrosses to the parental strains and analysis of (NON/ShiLt x NZO/Hl)F2 mice has led to the identification of a number of complex diabetes-predisposing ("diabesity") QTLs. Dr. Leiter's research group at The Jackson Laboratory is currently developing a series of nine recombinant congenic strains (RCS) made by backcrossing the (NZO/Hl x NON/ShiLt)F1 for two generations onto the NON/ShiLt background before inbreeding (~12% NZO/Hl, 88% NON/ShiLt genomes). Preliminary analysis indicates that body weight gains of all RCS are higher than NON/ShiLt, but none are as obese as NZO/Hl; some of these RCS develop NIDDM while others are resistant. These new strains will be useful to further analyze diabesity QTLs and as new models for type 2 (NIDDM) diabetes. An additional benefit of the RCS is better breeding performance than NZO/Hl.

Development

The New Zealand Obese (NZO) inbred mouse strain was initially selected for polygenic obesity. NZO mice share a common origin with New Zealand Black mice (NZB). M. Bielschowsky began inbreeding of outbred mice obtained from the Imp. Cancer Research Fund, London began at the University of Otago Medical School in 1948.

Selected References

Petkov PM; Cassell MA; Sargent EE; Donnelly CJ; Robinson P; Crew V; Asquith S; Haar RV; Wiles MV. 2004. Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse. Genomics 83(5):902-11. PubMed: 15081119 MGI: J:89298
Timmermans S; Van Montagu M; Libert C. 2017. Complete overview of protein-inactivating sequence variations in 36 sequenced mouse inbred strains. Proc Natl Acad Sci U S A 114(34):9158-9163. PubMed: 28784771 MGI: J:244295

View All References

Genetics

Pctp^R120H

Allele Symbol: Pctp^R120H

Allele Name	R120H
Allele Type	Spontaneous
Allele Synonym(s)
Gene Symbol and Name	Pctp, phosphatidylcholine transfer protein
Gene Synonym(s)	PC-TP; STARD2; StarD2; stARD2
Strain of Origin	NZO
Chromosome	11
Molecular Note	A G to A transition in exon 4 resulted in the arginine to histidine substitution at amino acid 120 in NZO, NZB/BINJ and NZW/LacJ strains. This mutation rendered the protein was inactive.

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Diabetes and Obesity Research
- Hyperglycemia
  - males
- Hyperinsulinemia
  - males
- Insulin Resistance
  - males
- Obesity With Diabetes
  - severe
- Type 2 Diabetes (NIDDM)
  - males
Reproductive Biology Research
- Fertility Defects
- Gonadal Tumors
  - granulosa cell tumors

Mammalian Phenotype Terms by Genotype

Genotype: Pctp^R120H/Pctp⁺
NZO

homeostasis/metabolism phenotype

abnormal lipid homeostasis
- phosphatidlycholine transfer activity is essentially absent in mutants
- this mutation abolishes the activity of phosphatidlycholine transfer protein

Phenotype Information

Festing Inbred Strain Characteristics: NZO

References

Petkov PM; Cassell MA; Sargent EE; Donnelly CJ; Robinson P; Crew V; Asquith S; Haar RV; Wiles MV. 2004. Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse. Genomics 83(5):902-11. PubMed: 15081119 MGI: J:89298
Timmermans S; Van Montagu M; Libert C. 2017. Complete overview of protein-inactivating sequence variations in 36 sequenced mouse inbred strains. Proc Natl Acad Sci U S A 114(34):9158-9163. PubMed: 28784771 MGI: J:244295

Additional References

Bielschowsky M; Goodall CM. 1970. Origin of inbred NZ mouse strains. Cancer Res 30(3):834-6. PubMed: 5425297 MGI: J:25459
Gates RJ; Hunt MI; Smith R; Lazarus NR. 1972. Return to normal of blood-glucose, plasma-insulin, and weight gain in New Zealand obese mice after implantation of islets of Langerhans. Lancet 2(777):567-70. PubMed: 4115740 MGI: J:35290
Haskell BD; Flurkey K; Duffy TM; Sargent EE; Leiter EH. 2002. The diabetes-prone NZO/HlLt strain. I. Immunophenotypic comparison to the related NZB/BlNJ and NZW/LacJ strains. Lab Invest 82(7):833-42. PubMed: 12118085 MGI: J:77828
Keane TM; Goodstadt L; Danecek P; White MA; Wong K; Yalcin B; Heger A; Agam A; Slater G; Goodson M; Furlotte NA; Eskin E; Nellaker C; Whitley H; Cleak J; Janowitz D; Hernandez-Pliego P; Edwards A; Belgard TG; Oliver PL; McIntyre RE; Bhomra A; Nicod J; Gan X; Yuan W; van der Weyden L; Steward CA; Bala S; Stalker J; Mott R; Durbin R; Jackson IJ; Czechanski A; Guerra-Assuncao JA; Donahue LR; Reinholdt LG; Payseur BA; Ponting CP; Birney E; Flint J; Adams DJ. 2011. Mouse genomic variation and its effect on phenotypes and gene regulation. Nature 477(7364):289-94. PubMed: 21921910 MGI: J:177037
Leiter EH; Reifsnyder PC; Flurkey K; Partke HJ; Junger E; Herberg L. 1998. NIDDM genes in mice: deleterious synergism by both parental genomes contributes to diabetogenic thresholds. Diabetes 47(8):1287-95. PubMed: 9703330 MGI: J:48957
Odet F; Pan W; Bell TA; Goodson SG; Stevans AM; Yun Z; Aylor DL; Kao CY; McMillan L; de Villena FP; O'Brien DA. 2015. The Founder Strains of the Collaborative Cross Express a Complex Combination of Advantageous and Deleterious Traits for Male Reproduction. G3 (Bethesda) 5(12):2671-83. PubMed: 26483008 MGI: J:244582
Rappaport H; Bielschowsky M; D'Ath EF; Goodall CM. 1971. Malignant lymphomas arising in Peyer's patches and other organs of untreated NZO-Bl mice. Cancer Res 31(12):2047-53. PubMed: 4941087 MGI: J:25462

Additional - Pctp^R120H related

Berndt A; Cario CL; Silva KA; Kennedy VE; Harrison DE; Paigen B; Sundberg JP. 2011. Identification of fat4 and tsc22d1 as novel candidate genes for spontaneous pulmonary adenomas. Cancer Res 71(17):5779-91. PubMed: 21764761 MGI: J:175528
Pan HJ; Agate DS; King BL; Wu MK; Roderick SL; Leiter EH; Cohen DE. 2006. A polymorphism in New Zealand inbred mouse strains that inactivates phosphatidylcholine transfer protein. FEBS Lett 580(25):5953-8. PubMed: 17046758 MGI: J:114974
Sundberg J. 2007. The Jackson Aging Center MGI Direct Data Submission :. MGI: J:122261

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Also Known As: New Zealand Obese

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