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Maternal and Paternal Obesity Differentially Impacts Body Weight and Glycemic Control in Male and Female Offspring

  • Author / Creator
    Aburasayn, Hanin
  • As the rate of obesity is increasing among children born to obese parents, our aim was to delineate how parental obesity promotes obesity risk in the offspring. A secondary aim was to determine if offspring born to obese parents would also be at risk of developing obesity-related metabolic dysfunction. Accordingly, the first project of this thesis work focused on maternal obesity and the prevalence of obesity and metabolic dysfunction in the offspring, which we assessed via recording of body weights, total adiposity, and overall glucose homeostasis. The second project of the thesis was explicitly focused on paternal obesity and how it may increase the risk of obesity and subsequent metabolic dysfunction in the developing offspring. To address our aims, C57BL/6J female mice were either fed a high fat diet (HFD) (60% kcal from lard) or a low fat diet (LFD) (10% kcal from lard) for 5 weeks. After 5 weeks of HFD or LFD feeding, they were bred with a 12- week old C57BL/6J male. All offspring were weaned onto a LFD and kept until 14 weeks of age. Magnetic resonance imaging (MRI) and metabolic cage analyses were utilized to assess overall adiposity and in vivo energy metabolism, while glucose homeostasis was also monitored by glucose and insulin tolerance testing. In addition, body weights were recorded frequently to assess their risk for obesity. Our results demonstrate that the female offspring born to an obese dam had an increase in body weight at weaning (3 weeks of age), whereas at 14 weeks of age they had a reduction in body weight versus offspring born to lean dams. However, fat mass was not different at any age range between our various groups of offspring. Last, measuring the expression of PGC1α in muscle, a key regulator of muscle energy metabolism, also revealed no differences between our various groups of offspring. In our second study, C57BL/6J male mice consumed a HFD or LFD for 5 weeks prior to breeding with a C57BL/6J lean female. The offspring were weaned onto either a LFD or HFD. We performed magnetic resonance imaging (MRI) and metabolic cage analyses to assess adiposity and energy metabolism respectively. In addition, glucose and insulin tolerance tests were conducted to assess glucose homeostasis. In addition, body weights were recorded frequently to assess the risk for obesity. To our surprise, only the LFD offspring showed a significantly heavier body weights at the age of weaning in both male/ female offspring; however, the HFD offspring group revealed similar body weight curves, regardless if the male parent was lean or obese. Surprisingly, offspring whose male parent was obese showed no differences in glucose tolerance and body weight gain compared to offspring counterparts whose male parent was lean. Last, we measured Ucp2 gene in muscle tissues of LFD offspring, a mitochondrial uncoupling protein that reduces ATP production and regulates thermogenesis. We observed a trend to higher Ucp2 expression in male offspring in which the male parent was obese versus lean. This trend was reversed in the female offspring. Taken together, one of the main conclusions of our research is that both maternal and paternal obesity do not increase the risk for obesity in the offspring.

  • Subjects / Keywords
  • Graduation date
    2018-11
  • Type of Item
    Thesis
  • Degree
    Master of Science
  • DOI
    https://doi.org/10.7939/R3RN30Q2R
  • License
    Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of these terms. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.