Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/90996
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Type: Journal article
Title: Paternal obesity induces metabolic and sperm disturbances in male offspring that are exacerbated by their exposure to an "obesogenic" diet
Author: Fullston, T.
McPherson, N.
Owens, J.
Kang, W.
Sandeman, L.
Lane, M.
Citation: Physiological Reports, 2015; 3(3):e12336-1-e12336-14
Publisher: Wiley
Issue Date: 2015
ISSN: 2051-817X
2051-817X
Statement of
Responsibility: 
Tod Fullston, Nicole O. McPherson, Julie A. Owens, Wan Xian Kang, Lauren Y. Sandeman & Michlle Lane
Abstract: Obesity and related comorbidities are becoming increasingly prevalent globally. In mice preconception paternal exposure to a high fat diet (HFD) impairs the metabolic and reproductive health of male offspring, despite their control diet (CD) consumption. However, offspring share lifestyle, including diet, with parents. We assessed if male offspring from HFD fathers have a heightened susceptibility to HFD-induced metabolic and reproductive derangements. This 2 × 2 design saw founder males (F0) and their offspring (F1) fed either a HFD or a nutritionally matched CD. Regardless of paternal diet, HFD fed male offspring had greater total body weight and adiposity. Offspring sired by a HFD male and fed a HFD were the heaviest, had the greatest adiposity and had the greatest concentration of serum cholesterol, triglyceride, HDL, and NEFA compared with CD sired/fed littermates. A synergistic increase in serum insulin was unmasked by both father/son HFD consumption, concomitant with increased sera glucose. Either a paternal or offspring HFD was associated with similar reductions to offspring sperm motility. Whereas sperm ROS concentrations and sperm-oocyte binding saw detrimental effects of both F0 HFD and F1 HFD with an interaction evident between both, culminating in the most impaired sperm parameters in this group. This indicates that metabolic and fertility disturbances in male offspring sired by HFD fathers are exacerbated by a "second-hit" of exposure to the same obesogenic environment postnatally. If translatable to human health, this suggests that adverse reproductive and metabolic outcomes may be amplified across generations through a shared calorie dense diet, relevant to the current worldwide obesity epidemic.
Keywords: Metabolic syndrome; obesogenic environment; paternal obesity; paternal programming; second‐hit; subfertility
Rights: © 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
RMID: 0030025489
DOI: 10.14814/phy2.12336
Appears in Collections:Paediatrics publications

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