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The effect of maternal high-fat/high-sugar diet on offspring oocytes and early embryo development.

ABSTRACT: Observational human data and several lines of animal experimental data indicate that maternal obesity impairs offspring health. Here, we comprehensively tested the model that maternal obesity causes defects in the next three generations of oocytes and embryos. We exposed female F0 mice to a high-fat/high-sugar (HF/HS) diet for 6 weeks before conception until weaning. Sires, F1 offspring and all subsequent generations were fed control chow diet. Oocytes from F1, F2 and F3 offspring of obese mothers had lower mitochondrial mass and less ATP and citrate than oocytes from offspring of control mothers. F0 blastocysts from HF/HS-exposed mice, but not F1 and F2 blastocysts, had lower mitochondrial mass and membrane potential, less citrate and ATP and smaller total cell number than F0 blastocysts from control mothers. Finally, supplementation of IVF media with the anti-oxidant mito-esculetin partially prevented the oocyte mitochondrial effects caused by maternal HF/HS diet. Our results support the idea that maternal obesity impairs offspring oocyte quality and suggest that antioxidant supplementation should be tested as a means to improve IVF outcomes for obese women.

SUBMITTER: Andreas E

PROVIDER: S-EPMC6884416 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature

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The effect of maternal high-fat/high-sugar diet on offspring oocytes and early embryo development.

Andreas E E Reid M M Zhang W W Moley K H KH

Molecular human reproduction 20191101 11

Observational human data and several lines of animal experimental data indicate that maternal obesity impairs offspring health. Here, we comprehensively tested the model that maternal obesity causes defects in the next three generations of oocytes and embryos. We exposed female F0 mice to a high-fat/high-sugar (HF/HS) diet for 6 weeks before conception until weaning. Sires, F1 offspring and all subsequent generations were fed control chow diet. Oocytes from F1, F2 and F3 offspring of obese mothe ...[more]

PMID: 31588490

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Project description:Maternal diabetes-induced fetal programming predisposes offspring to type 2 diabetes, cardiovascular disease, and obesity in adulthood. However, lifelong health and disease trajectories depend on several factors and nutrition is one of the main ones. We intend to understand the role of maternal diabetes-induced fetal programming and its association with a high-fat diet during lifelong in the female F1 generation focusing on reproductive outcomes and the possible changes in physiological systems during pregnancy as well as the repercussions on the F2 generation at birth. For this, we composed four groups: F1 female pups from control (OC) or from diabetic dams (OD) and fed with standard (SD) or high-fat diet from weaning to full-term pregnancy. During pregnancy, glucose intolerance and insulin sensitivity were evaluated. In a full-term pregnancy, the maternal blood and liver were collected to evaluate redox status markers. The maternal blood, placental tissue, and fetal blood (pool) were collected to evaluate adiponectin and leptin levels. Maternal reproductive parameters were evaluated as well. Maternal diabetes and high-fat diet consumption, in isolation, were both responsible for increased infertility rates and fasting glucose levels in the F1 generation and fetal growth restriction in the F2 generation. The association of both conditions showed, in addition to those, increased lipoperoxidation in maternal erythrocytes, regardless of the increased endogenous antioxidant enzyme activities, glucose intolerance, decreased number of implantation sites and live fetuses, decreased litter, fetal and placental weight, increased preimplantation losses, and increased fetal leptin serum levels. Thus, our findings show that fetal programming caused by maternal diabetes or lifelong high-fat diet consumption leads to similar repercussions in pregnant rats. In addition, the association of both conditions was responsible for glucose intolerance and oxidative stress in the first generation and increased fetal leptin levels in the second generation. Thus, our findings show both the F1 and F2 generations harmed health after maternal hyperglycemic intrauterine environment and exposure to a high-fat diet from weaning until the end of pregnancy.

Project description:A maternal high-fat diet (HFD) has been shown to exert deleterious effects on fetal programming by impairing embryo growth, and exerts a long-term effect on the health of offspring. The present study aimed to evaluate the effect of a maternal HFD on the ovaries of offspring from the perspective of oxidative stress. Female C57BL/6J mice were randomly assigned to four groups fed various HFDs during the preconception (4 weeks) and gestation-lactation periods. Offspring were fed a normal diet after weaning, and serum and ovaries were collected at 10 weeks of age. The developmental status of follicles was observed using hematoxylin and eosin staining. The serum oxidative stress levels and insulin resistance were detected using ELISA test kits. The expression of phosphorylated form of H2AX histone variant (γH2AX), forkhead box protein O3a (FOXO3a), Bcl-2-like protein 11 (Bim)and insulin-like growth factor (IGF)-1 in ovarian tissue was analyzed using reverse transcription-quantitative PCR and western blot analyses to further explore the pathogenic mechanism. Prenatal exposure to a maternal HFD resulted in a reduced number of primordial and preantral follicles in the ovaries of offspring. Exposure to an HFD in the preconception period exerted a greater effect on the offspring compared with exposure to an HFD in the gestation-lactation period. A reduction in fat intake during the preconception, gestation and lactation periods significantly reduced the associated adverse outcomes. The expression of genes (FOXO3a, IGF-1, γH2AX and Bim) involved in oxidative stress showed a decreasing trend (high-fat/high-fat>high-fat/control>control/high-fat >control/control) in the ovaries of offspring. Overall, HFD exposure during the preconception period exerted a greater effect on offspring compared with HFD exposure during the gestation-lactation period. The long-term effect on follicular growth and development may be associated with increased oxidative stress and the activation of the insulin/PI3K/Akt pathway.

Dataset Information

The effect of maternal high-fat/high-sugar diet on offspring oocytes and early embryo development.

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The effect of maternal high-fat/high-sugar diet on offspring oocytes and early embryo development.

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