Saben 2016 Cell Rep

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Saben JL, Boudoures AL, Asghar Z, Thompson A, Drury A, Zhang W, Chi M, Cusumano A, Scheaffer S, Moley KH (2016) Maternal metabolic syndrome programs mitochondrial dysfunction via germline changes across three generations. Cell Rep 16:1-8.

» PMID: 27320925 Open Access

Saben JL, Boudoures AL, Asghar Z, Thompson A, Drury A, Zhang W, Chi M, Cusumano A, Scheaffer S, Moley KH (2016) Cell Rep

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.

Copyright © 2016. Published by Elsevier Inc.


Labels: MiParea: Respiration, mt-Biogenesis;mt-density, mt-Structure;fission;fusion, mtDNA;mt-genetics, Exercise physiology;nutrition;life style  Pathology: Obesity 

Organism: Mouse  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue  Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase 

Coupling state: LEAK, OXPHOS, ET  Pathway: N, NS  HRR: Oxygraph-2k 

2016-08