A Systematic Review of the Effects of High-Fat Diet Exposure on Oocyte and Follicular Quality: A Molecular Point of View

Abstract

Worldwide, infertility affects between 10 and 15% of reproductive-aged couples. Female infertility represents an increasing health issue, principally in developing countries, as the current inclinations of delaying pregnancy beyond 35 years of age significantly decrease fertility rates. Female infertility, commonly imputable to ovulation disorders, can be influenced by several factors, including congenital malformations, hormonal dysfunction, and individual lifestyle choices, such as smoking cigarettes, stress, drug use and physical activity. Moreover, diet-related elements play an important role in the regulation of ovulation. Modern types of diet that encourage a high fat intake exert a particularly negative effect on ovulation, affecting the safety of gametes and the implantation of a healthy embryo. Identifying and understanding the cellular and molecular mechanisms responsible for diet-associated infertility might help clarify the confounding multifaceted elements of infertility and uncover novel, potentially curative treatments. In this view, this systematic revision of literature will summarize the current body of knowledge of the potential effect of high-fat diet (HFD) exposure on oocyte and follicular quality and consequent female reproductive function, with particular reference to molecular mechanisms and pathways. Inflammation, oxidative stress, gene expression and epigenetics represent the main mechanisms associated with mammal folliculogenesis and oogenesis.

Cuban Policosanol (Raydel®) Potently Protects the Liver, Ovary, and Testis with an Improvement in Dyslipidemia in Hyperlipidemic Zebrafish: A Comparative Study with Three Chinese Policosanols

“…The current results showed that hyperlipidemia and fatty liver changes are also linked to severe impairments in the reproductive organs ( Figure 7 , Figure 8 and Figure 9 ). HCD supplementation caused a decrease in the mature vitellogenic stage of approximately 2.7%, while the ND group showed 6.5%, indicating that elevated oxidative stress caused by hyperlipidemia inhibited oocyte maturation, as reported elsewhere [ 43 , 44 ]. In the current study, however, the co-supplementation of Cuban policosanol resulted in the largest increase in early-vitellogenic and mature-vitellogenic oocytes, indicating enhanced oocyte maturation and folliculogenesis.…”

High-Fat Diet and Female Fertility across Lifespan: A Comparative Lesson from Mammal Models

“…In this context, diet, including hypercaloric nutrition, may result in metabolic derangements and in body weight increase which promote obesity, an increase in ovarian dysfunction, and the risk of infertility. Indeed, obesity perturbates the hypothalamic–pituitary–ovarian axis dialogue through an inhibitory action exerted by the adipose tissue that has a recognized critical role in maintaining the endocrine/paracrine control of the gonads, with the aim of synchronously regulating the follicle–oocyte development over time until ovulation [ 2 , 3 ]. To date, many research studies that have clarified the mechanisms behind high-fat-related infertility in mammals were carried out in experimental animal models [ 4 , 5 ].…”

Inflammation mediates the effect of adiposity and lipid metabolism indicators on the embryogenesis of PCOS women undergoing in vitro fertilization/intracytoplasmic sperm injection

“…Pro-inflammatory mediators may inhibit insulin receptors, reduce insulin sensitivity and aggravate IR, consequently worsening reproductive dysfunction ( 41 , 42 ). Obesity can induce higher levels of inflammatory mediators in the ovary, which may cause irreversible damage to the oogenesis and ovary function ( 21 , 43 ). Oxidative stress, closely related to inflammatory response, can also lead to oocyte apoptosis and ovarian dysfunction ( 44 ).…”

“…Oxidative stress, closely related to inflammatory response, can also lead to oocyte apoptosis and ovarian dysfunction ( 44 ). The change in obesity-induced inflammation and oxidative stress pathways may alter the expression of genes related to oocyte quality, thus adversely affecting the subsequent embryogenesis ( 21 ). Furthermore, the NLRP3 inflammasome and the chemokine decoy receptor D6, two representative uterine inflammatory mediators, may disturb the maternal–fetal interface with the subsequent occurrence and progress of obstetric complications ( 22 ).…”

“…In PCOS women, obesity, pro-inflammatory response, oxidative stress, IR, hyperinsulinemia, and hyperandrogenism interact to form a vicious cycle ( 7 , 19 ). Inflammation has been elucidated to cause damage to oocyte and follicular quality ( 21 ). A uterine hyperinflammatory state of PCOS women may contribute to placental insufficiency and obstetric complications ( 22 ).…”