Abstract
Mammalian cloning using somatic cells has been accomplished successfully in several species, and its potential basic, clinical and therapeutic applications are being pursued on many fronts. Determining the long-term effects of cloning on offspring is crucial for consideration of future application of the technique. Although full-term development of animals cloned from adult somatic cells has been reported, problems in the resulting progeny indicate that the cloning procedure may not produce animals that are phenotypically identical to their cell donor. We used a mouse model to take advantage of its short generation time and lifespan. Here we report that the increased body weight of cloned B6C3F1 female mice reflects an increase of body fat in addition to a larger body size, and that these mice share many characteristics consistent with obesity. We also show that the obese phenotype is not transmitted to offspring generated by mating male and female cloned mice.
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Acknowledgements
We thank K. Ellis, L.Y. Ma, T. Osada and K. Smith for their contributions to this study. This work was supported by National Institutes of Health grants DK-48061 to R.R.S. and DK-17844 to S.C.W., the Victoria S. and Bradley L. Geist Foundation, the Kosasa Family Foundation and grants from the Katherine and Harold Castle Foundation to R.Y. The Obesity Research Center at the University of Cincinnati is supported by Procter & Gamble.
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Tamashiro, K., Wakayama, T., Akutsu, H. et al. Cloned mice have an obese phenotype not transmitted to their offspring. Nat Med 8, 262–267 (2002). https://doi.org/10.1038/nm0302-262
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DOI: https://doi.org/10.1038/nm0302-262
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