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Published on: May 5, 2018
High-Fat Diet during Mouse Pregnancy Impairs Fetal Heart Development
Kaixin Ge1, Diyaerjiang Aierken1, Defang Deng2
1Department of Cardiac Surgery, Zhongshan Hospital, Fudan University.
Insights
Maternal high-fat diet (HFD) during pregnancy causes offspring growth restriction and impaired heart development. These cardiac defects persist postnatally, linked to TP53-regulated cell cycle arrest.
Area of Science:
- Developmental Biology
- Cardiovascular Science
- Nutritional Science
Background:
- Maternal overnutrition is linked to adverse offspring outcomes.
- Specific impacts of gestational high-fat diet (HFD) on fetal development are not fully understood.
Purpose of the Study:
- To investigate the effects of gestational HFD on neonatal organ development and cardiomyocyte cell cycle activity in mice.
- To identify molecular mechanisms underlying HFD-induced developmental defects in offspring.
Main Methods:
- Utilized a high-fat diet (HFD) mouse model.
- Assessed offspring development, organ growth, and cardiomyocyte proliferation.
- Performed RNA sequencing on postnatal day 0 (P0) cardiomyocytes.
Main Results:
- Gestational HFD led to offspring growth retardation and reduced cardiomyocyte proliferation.
- RNA sequencing revealed impaired fatty acid metabolism, increased inflammation, and TP53-regulated cell cycle arrest in cardiomyocytes.
- Postnatal recovery through normal lactation and feeding was insufficient to reverse cardiac developmental defects.
Conclusions:
- Maternal HFD during gestation profoundly impacts offspring heart development.
- TP53-dependent cell cycle arrest is implicated in HFD-induced cardiac defects.
- Early nutritional interventions cannot fully correct gestational HFD-induced cardiovascular abnormalities.
Abstract:
Maternal overnutrition correlates with detrimental outcomes in offspring. However, the specific effects of gestational exposure to a high-fat diet (HFD) on fetal development remain unclear. This study aimed to elucidate the developmental phenotypes of neonatal organs and cardiomyocytes of mice exposed to gestational HFD, revealing growth retardation and a notable reduction in cardiomyocyte cell cycle activity. In this study, an HFD model was used to investigate the effects of maternal HFD on offspring development. Defective development was observed in the offspring, and severe restriction of cell proliferation was noted in the neonatal organs as a result of maternal HFD. Based on this evidence, we detected a reduction in cardiomyocyte proliferation in offspring exposed to maternal HFD. Moreover, RNA sequencing analysis revealed that HFD diminished fatty acid metabolism, enhanced the inflammatory response, and upregulated the transcription of genes involved in Tp53-regulated cell cycle arrest in postnatal day 0 (P0) cardiomyocytes. Furthermore, our results showed that the effects of the maternal diet during gestation are profound and normal lactation and feeding after delivery cannot help adult offspring recover from defective heart development. These findings highlight the diverse pathways affected by maternal HFD, particularly implicating a potential TP53-dependent mechanism contributing to cardiac defects in offspring.
