Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/102392
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Type: Journal article
Title: Sperm microRNA content is altered in a mouse model of male obesity, but the same suite of microRNAs are not altered in offspring's sperm
Author: Fullston, T.
Ohlsson-Teague, E.
Print, C.
Sandeman, L.
Lane, M.
Citation: PLoS One, 2016; 11(11):e0166076-1-e0166076-18
Publisher: PLOS ONE
Issue Date: 2016
ISSN: 1932-6203
1932-6203
Statement of
Responsibility: 
Tod Fullston, E. Maria C. Ohlsson-Teague, Cristin G. Print, Lauren Y. Sandeman, Michelle Lane
Abstract: The prevalence of obesity is increasing worldwide and has tripled in men of reproductive age since the 1970s. Concerningly, obesity is not only comorbid with other chronic diseases, but there is mounting evidence that it increases the non-communicable disease load in their children (eg mortality, obesity, autism). Animal studies have demonstrated that paternal obesity increases the risk of metabolic (eg glucose metabolism defects, obesity) and reproductive disorders in offspring. Epigenetic changes within sperm are clear mechanistic candidates that are associated with both changes to the father’s environment and offspring phenotype. Specifically there is emerging evidence that a father’s sperm microRNA content both responds to paternal environmental cues and alters the gene expression profile and subsequent development of the early embryo. We used a mouse model of high fat diet (HFD) induced obesity to investigate whether male obesity could modulate sperm microRNA content. We also investigated whether this alteration to a father’s sperm microRNA content lead to a similar change in the sperm of male offspring. Our investigations were initially guided by a Taqman PCR array, which indicated the differential abundance of 28 sperm borne microRNAs in HFD mice. qPCR confirmation in a much larger cohort of founder males demonstrated that 13 of these microRNAs were differentially abundant (11 up-regulated; 2 down-regulated) due to HFD feeding. Despite metabolic and reproductive phenotypes also being observed in grand-offspring fathered via the male offspring lineage, there was no evidence that any of the 13 microRNAs were also dysregulated in male offspring sperm. This was presumably due to the variation seen within both groups of offspring and suggests other mechanisms might act between offspring and grand-offspring. Thus 13 sperm borne microRNAs are modulated by a father’s HFD and the presumed transfer of this altered microRNA payload to the embryo at fertilisation potentially acts to alter the embryonic molecular makeup post-fertilisation, altering its growth trajectory, ultimately affecting adult offspring phenotype and may contribute to paternal programming.
Keywords: Spermatozoa; Animals; Mice, Inbred C57BL; Mice; Obesity; Disease Models, Animal; MicroRNAs; Fathers; Epigenesis, Genetic; Reproduction; Fertilization; Male; Adiposity; Transcriptome; Diet, High-Fat
Rights: © 2016 Fullston et al. This is an open access article distributed under the terms of the Creative Commons Attribution License [BY 4.0], which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
RMID: 0030057648
DOI: 10.1371/journal.pone.0166076
Grant ID: http://purl.org/au-research/grants/nhmrc/1042089
http://purl.org/au-research/grants/nhmrc/1022882
http://purl.org/au-research/grants/nhmrc/1036561
Appears in Collections:Medicine publications

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