Maternal and paternal obesity differentially reprogram the ovarian mitochondrial biogenesis of F1 female rats

Abstract

Obesity has harmful consequences on reproductive outcomes and the rapid increase in obesity is assumed to be influenced by epigenetics and trans-generation effects. Our study aimed to explore the effect of maternal and/or paternal obesity on the ovarian tissues of the first-generation female offspring in rats. The study was conducted on 40 adult Wistar albino rats (20 males and 20 females). Obesity was induced by feeding them an obesogenic diet for 3 months. The pregnancy was induced in the females by mating with males in four combinations: healthy mother with healthy father (control parents, CP), healthy mother with obese fathers (OF), obese mothers with healthy father (OM), and obese mother with obese father (obese parents, OP). After delivery, the female offspring at two months were sacrificed, and the blood and ovarian tissues were collected to assess the studied parameters. Our result showed differential impacts of maternal and paternal obesity on the ovarian health of the female offspring. The female offspring of obese OM or OP showed early signs of obesity. These metabolic abnormalities were associated with signs of ovarian lesions, impaired folliculogenesis, and decreased oocyte quality and also showed significant alterations in mitochondrial biogenesis, redox status, inflammation, and microRNAs expression (miR-149 and miR-494). In conclusion, altered ovarian expression of microRNAs and associated impaired mitochondrial biogenesis pathways may be the root causes for the observed intergeneration transmission of the obesogenic phenotype.

The impact of offspring and maternal obesogenic diets on adult offspring oocyte mitochondrial morphology in primordial and preantral follicles

“…Moreover, children born to obese mothers have increased risk of developing metabolic syndrome, including obesity and diabetes [ 3 ], and are thus more prone to the development of metabolic diseases later in life [ 4 – 7 ]. A few studies in diet-induced obese mouse models suggested that maternal obesity increases the risk of reproductive disorders in the offspring as well [ 8 – 10 ]. Since children mostly follow the same lifestyle and dietary habits of their parents [ 11 ], some of the reported effects of maternal obesity on offspring health and fertility can be, at least in part, due to direct effects of consuming obesogenic (OB) diets after ablactation.…”

Resveratrol ameliorates mitochondrial biogenesis and reproductive outcomes in women with polycystic ovary syndrome undergoing assisted reproduction: a randomized, triple-blind, placebo-controlled clinical trial

“…The abundance of mitochondria in the granulosa cells (GCs) surrounding a specific oocyte is positively correlated with oocyte maturation, fertilization, and successful embryo development [ 3 ]. The mitochondrial biogenesis pathway is a fundamental factor in follicular development [ 4 ]. Mitochondrial biogenesis involves the expansion and division of existing mitochondria [ 5 ].…”