Maternal obesity affects gene expression and cellular development in fetal brains
Ewa K Stachowiak1, Saji Oommen, Vihas T Vasu
1University at Buffalo, State University of New York, Buffalo, NY, USA.
Insights
Maternal obesity in rats alters fetal brain development, leading to gene expression changes and impaired neuronal growth. This may predispose offspring to metabolic and neurological disorders later in life.
Area of Science:
- Developmental biology
- Neuroscience
- Metabolic disorders
Background:
- High carbohydrate (HC) milk formula induces chronic hyperinsulinemia and obesity in female rat neonates.
- Maternal obesity during gestation creates an adverse intrauterine environment, impacting fetal development and transferring the HC phenotype to offspring.
Purpose of the Study:
- To investigate global gene expression patterns in term HC fetal brains.
- To examine cellular development in term HC fetal brains exposed to an adverse intrauterine environment.
Main Methods:
- GeneChip analysis of total RNA from fetal brains for gene expression profiling.
- Immunohistochemical analysis of fetal brain slices to assess cellular development.
Main Results:
- Gene expression profiling revealed alterations in gene clusters potentially contributing to the maternal phenotype transfer.
- Immunohistochemistry showed reduced proliferation and neuronal maturation in stem-like cells within HC fetal brains.
Conclusions:
- Maternal obesity during pregnancy can disrupt fetal brain developmental programming.
- These developmental alterations may contribute to metabolic syndrome and neurological disorders in offspring.
Objectives:
Female rat neonates reared on a high carbohydrate (HC) milk formula developed chronic hyperinsulinemia and adult-onset obesity (HC phenotype). Furthermore, we have shown that fetal development in the HC intrauterine environment (maternal obesity complicated with hyperinsulinemia, hyperleptinemia, and increased levels of proinflammatory markers) resulted in increased levels of serum insulin and leptin in term HC fetuses and the spontaneous transfer of the HC phenotype to the adult offspring. The objectives of this study are to identify changes in global gene expression pattern and cellular development in term HC fetal brains in response to growth in the adverse intrauterine environment of the obese HC female rat.
Methods:
GeneChip analysis was performed on total RNA obtained from fetal brains for global gene expression studies and immunohistochemical analysis was performed on fetal brain slices for investigation of cellular development in term HC fetal brains.
Results:
Gene expression profiling identified changes in several clusters of genes that could contribute to the transfer of the maternal phenotype (chronic hyperinsulinemia and adult-onset obesity) to the HC offspring. Immunohistochemical analysis indicated diminished proliferation and neuronal maturation of stem-like cells lining the third ventricle, hypothalamic region, and the cerebral cortex in HC fetal brains.
Discussion:
These results suggest that maternal obesity during pregnancy could alter the developmental program of specific fetal brain cell-networks. These defects could underlie pathologies such as metabolic syndrome and possibly some neurological disorders in the offspring at a later age.
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