Compensatory responses in mice carrying a null mutation for Ins1 or Ins2.

@article{Leroux2001CompensatoryRI,
  title={Compensatory responses in mice carrying a null mutation for Ins1 or Ins2.},
  author={L. D. Leroux and Pierrette Desbois and Luciane Lamotte and Bertrand Duvilli{\'e} and Nathalie Cordonnier and Malene Jackerott and Jacques Jami and Danielle Bucchini and Rajiv L. Joshi},
  journal={Diabetes},
  year={2001},
  volume={50 Suppl 1},
  pages={S150-3}
}
Intrauterine growth retardation and postnatal acute diabetes result from insulin deficiency in double homozygous null mutants for Ins1 and Ins2 (Duvillié B, et al., Proc. Natl. Acad. Sci. USA 94:5137-5140, 1997). The characterization of single homozygous null mutants for Ins1 or Ins2 is described here. Neither kind of mutant mice was diabetic. Immunocytochemical analysis of the islets showed normal distribution of the endocrine cells producing insulin, glucagon, somatostatin, or pancreatic… CONTINUE READING

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