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Cell Rep. 2016 Jun 28;16(1):1-8. doi: 10.1016/j.celrep.2016.05.065. Epub 2016 Jun 16.

Maternal Metabolic Syndrome Programs Mitochondrial Dysfunction via Germline Changes across Three Generations.

Author information

1
Department of Obstetrics and Gynecology, Washington University School of Medicine, 425 South Euclid Avenue, St. Louis, MO 63110, USA.
2
Department of Obstetrics and Gynecology, Washington University School of Medicine, 425 South Euclid Avenue, St. Louis, MO 63110, USA. Electronic address: moleyk@wustl.edu.

Abstract

Maternal obesity impairs offspring health, but the responsible mechanisms are not fully established. To address this question, we fed female mice a high-fat/high-sugar diet from before conception until weaning and then followed the outcomes in the next three generations of offspring, all fed a control diet. We observed that female offspring born to obese mothers had impaired peripheral insulin signaling that was associated with mitochondrial dysfunction and altered mitochondrial dynamic and complex proteins in skeletal muscle. This mitochondrial phenotype persisted through the female germline and was passed down to the second and third generations. Our results indicate that maternal programming of metabolic disease can be passed through the female germline and that the transfer of aberrant oocyte mitochondria to subsequent generations may contribute to the increased risk for developing insulin resistance.

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PMID:
27320925
PMCID:
PMC4957639
DOI:
10.1016/j.celrep.2016.05.065
[Indexed for MEDLINE]
Free PMC Article

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