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Inbred Strains of Mice: NZO


Inbr: F128 (Wehi). Agouti. Genet: +. Origin: see NZB.


Intermediate to low incidence of ovarian granulosa cell tumours (Bielschowsky and D'Ath, 1973). Median life-span about 460 days in males and 530 days in females. High incidence (15-20%) of malignant lymphomas of Peyer's patches and high incidence of duodenal and lung tumours (Goodall et al., 1972., 197; Rappaport et al., 1971 al., 1971).

Very obese. Fat collects mainly in the abdomen, starting about 4 weeks, although divergence of growth curves is not detectable before about 2-4 months. At maturity 50-74% of body weight is fat. Animals are hyperglycaemic but not hyperinsulinaemic (Bray and York, 1971). Blood glucose levels, plasma insulin levels, body weight and glucose tolerance return to normal after implantation of pancreatic islets from normal albino mice. The genetic lesion therefore appears to be situated within the islets of Langerhans (Gates et al., 1972., 1972). Obesity is largely caused by an increase in adipose cell numbers, although cell size is slightly increased (Johnson and Hirsch, 1972). Obesity may be at least partly due to an abnormality in the cyclic AMP system which controls lipolysis in adipose tissue (Lovell-Smith and Sneyd, 1973). Obese syndrome also reviewed by Stauffacher et al. (1971). Develop non-insulin-dependent diabetes mellitus (NIDDM) with active liver glycogen synthase (GS) reduced to 54% and 36% in neonates and adults, respectively. However, total GS was 65% higher in adults than in NZC controls. Glycogen phosphorylase was not different from NZC controls (Thorburn et al, 1995). Increased hepatic glucose production is present at an early age and is associated with impared suppression of the gluconeogenic enzyme fructose-1,6-bisphosphatase (Andrikopoulos et al, 1996).

Andrikopoulos S., Rosella G., Kaczmarczyk S. J., Zajac J. D., and Proietto J. (1996) Impaired regulation of hepatic fructose-1,6-bisphosphatase in the New Zealand obese mouse: An acquired defect. Metabolism: Clinical and Experimental 45, 622-626.

Bielschowsky M. and D'Ath E. F. (1973) Spontaneous granulosa cell tumours in mice of strains NZC/Bl, NZO/Bl, NZY/Bl and NZB/Bl. Pathology 5, 303-310.

Bray G. A. and York D. A. (1971) Genetically transmitted obesity in rodents. Physiol. Rev. 51, 598-646.

Gates R. J., Hunt M. I., Smith R., and Lazarus N. R. (1972) Return to normal of blood-glucose, plasma-insulin, and weight gain in New Zea1and obese mice after implantation of islets of Langerhans. The Lancet ii, 567-570.

Goodall C. M., Bielschowsky M., and Forster D. R. (1972) Incidence and metastatic pattern of lymphoreticular neoplasms in untreated NZO/Bl mice. Lab. Anim. 6, 85-94.

Johnson P. R. and Hirsch J. (1972) Cellularity of adipose depots in six strains of genetically obese mice. J. Lipid Res. 13, 2-11.

Lovell-Smith C. J. and Sneyd J. G. T. (1973) Lipolysis and adenosine 3', 5'- cyclic monophosphate in adipose tissue of the New 2ealand obese mouse. J. Endocrinol. 56, 1-11.

Rappaport H., Bielschowsky M., D'Ath E. F., and Goodall C. M. (1971) Malignant lymphomas arising in Peyer's patches and other organs of untreated NZ0/Bl mice. Cancer Res. 31, 2047-2053.

Stauffacher W., Orci L., Cameron D. P., Burr I. M., and Renold A. E. (1971) Spontaneous hyperglycemia and/or obesity in laboratory rodents: an example of the possible usefulness of animal disease models with both genetic and environmental components. Recent Prog. Horm. Res. 27, 41-91.

Thorburn A., Andrikopoulos S., and Proietto J. (1995) Defects in liver and muscle glycogen metabolism in neonatal and adult New Zealand obese mice. Metabolism: Clinical and Experimental 44, 1298-1302.

Updated 9 Apr. 1998
Michael FW Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester, UK

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