Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/120401
Type: Thesis
Title: Dietary interventions for improving fertility
Author: Bermudez Gonzalez, Macarena
Issue Date: 2018
School/Discipline: Adelaide Medical School
Abstract: Obesity has dramatically increased in the population in the last few decades, and data from the Australian Bureau of Statistics National Health Survey indicates that currently approximately half of the women in Australia are overweight or obese. The fact that many of these women are in their reproductive years is concerning. Obesity increases the risk of developing chronic diseases as well as having a negative effect on women’s reproductive health, influencing the prevalence of subfertility, infertility and pregnancy complications. Polycystic Ovary Syndrome (PCOS) is the most common reproductive disorder in women and it is closely related to obesity. It is characterized by acyclicity, anovulation and increased levels of androgens in blood, as well as decreased rates of pregnancy. Increased BMI has been associated with dysregulated menstrual cycles, anovulation or oligo-ovulation, and lower pregnancy rates. Recent evidence suggests that obesity causes the initiation of a pro-inflammatory state that extends to the adipose, liver, and muscle tissues. The increased release of proinflammatory cytokines from adipose tissue, such as interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α), induces lipolysis, enhances cytokine release, and promotes insulin resistance. At the cellular level, it is characterized by mitochondrial dysfunction and the activation of stress pathways, namely Endoplasmic reticulum (ER)-stress and the Heat Shock Response (HSR). The different stress responses constitute a complex network that interacts not only with nascent polypeptides and stress-denatured proteins, but also with metabolic (insulin), hormonal (steroid hormones and their receptors) and immunological pathways (antigen presentation). That these pathways also affect ovarian function makes HSP a potential target for therapeutic interventions in obesity. However, it is still not clear how obesity influences the ovarian environment, and how this affects stress pathways in ovarian cells, as well as its impact on oocyte homeostasis and the development of the preimplantation embryo. Thus, I will explore how different factors impact the obesity phenotype in female mice, with special emphasis on ovarian function and the expression of stress responses in ovarian cells, and ultimately how they affect oocyte quality and developmental potential. For this, I will be using three different mouse models of obesity, namely a Dihydrotestosterone (DHT) -induced PCOS model, a High fat diet (HFD) -induced model and a High Sugar High Fat combination diet. Finally, I will determine if specific chaperone-inducing micronutrients can promote the induction of these cytoprotective HSP and/or normalize ER stress, in order to identify a natural fertility-protective diet.
Advisor: Robker, Rebecca
Wu, Linda
Dissertation Note: Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2019
Keywords: Obesity
ovary
oocyte
heat shock protein
high fat diet
curcumin
opuntia
Provenance: This electronic version is made publicly available by the University of Adelaide in accordance with its open access policy for student theses. Copyright in this thesis remains with the author. This thesis may incorporate third party material which has been used by the author pursuant to Fair Dealing exceptions. If you are the owner of any included third party copyright material you wish to be removed from this electronic version, please complete the take down form located at: http://www.adelaide.edu.au/legals
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