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Mice generated by assisted reproductive techniques exhibit altered glucose metabolism
Cloning by somatic cell nuclear transfer and assisted reproductive techniques (ART) have been associated with an increased occurrence of phenotypic abnormalities in rodents. We previously demonstrated that female mice cloned from adult somatic cells become obese in adulthood. Here, we sought to pars...
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Published in: | Appetite 2007-07, Vol.49 (1), p.329-329 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Online Access: | Get full text |
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Summary: | Cloning by somatic cell nuclear transfer and assisted reproductive techniques (ART) have been associated with an increased occurrence of phenotypic abnormalities in rodents. We previously demonstrated that female mice cloned from adult somatic cells become obese in adulthood. Here, we sought to parse out the effects of cloning from those caused by in vitro culture and manipulation of embryos by comparing Stock controls, mice that were produced through natural matings, with offspring generated by in vitro fertilization (IVF, effect of in vitro culture) and intracytoplasmic sperm injection (ICSI, effect of in vitro culture + mechanical injection). All pups were cross-fostered at birth. In contrast to clones, placental hypertrophy was not seen in ICSI and IVF births, although birth weights of ICSI and IVF pups were significantly higher than those of Stock mice. At 8 weeks of age, there was no difference in food intake although ICSI and IVF weighed slightly more than Stock mice. In a glucose tolerance test (20% glucose solution, 1.5
mg/g, i.p.), IVF, ICSI and Stock mice had a similar peak in blood glucose at 15
min, but glucose levels remained significantly elevated at 30, 45 and 60
min in ICSI and IVF mice, before returning to baseline levels at 120
min. These results suggest that in vitro culture and manipulation of embryos may account for some of the differences seen in ART and cloned mice, and that impaired glucose tolerance occurs prior to the onset of obesity. Support: DK068273 (R.R.S.) and NS007453 (K.A.S.). |
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ISSN: | 0195-6663 1095-8304 |
DOI: | 10.1016/j.appet.2007.03.185 |