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Published on: February 26, 2014
Maternal obesity impairs hippocampal BDNF production and spatial learning performance in young mouse offspring
Yusuke Tozuka1, Mami Kumon, Etsuko Wada
1Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan.
Insights
Maternal obesity from a high-fat diet impairs offspring hippocampal development and spatial learning. This is linked to reduced brain-derived neurotrophic factor (BDNF) and increased oxidative stress in young mice.
Area of Science:
- Neuroscience
- Developmental Biology
- Metabolic Research
Background:
- Maternal obesity is linked to offspring health risks, including metabolic syndrome.
- Emerging evidence suggests maternal obesity impacts offspring neural development.
- The specific effects on hippocampal development require further investigation.
Purpose of the Study:
- To investigate the impact of diet-induced maternal obesity on hippocampal development and function in mouse offspring.
- To assess changes in brain-derived neurotrophic factor (BDNF) and oxidative stress markers.
- To evaluate hippocampus-dependent cognitive functions, particularly spatial learning and memory.
Main Methods:
- Adult female mice were fed normal or high-fat diets before and during pregnancy/lactation.
- Offspring hippocampus was analyzed for lipid peroxidation and BDNF levels.
- Retroviral labeling assessed dendritic arborization of hippocampal neurons.
- Barnes maze test evaluated spatial learning and memory acquisition.
Main Results:
- High-fat diet (HFD) offspring exhibited increased hippocampal lipid peroxidation.
- HFD offspring showed reduced hippocampal brain-derived neurotrophic factor (BDNF) levels.
- Impaired dendritic arborization and deficits in spatial learning acquisition were observed in young HFD offspring.
Conclusions:
- Diet-induced maternal obesity negatively impacts hippocampal development and function in offspring.
- Reduced BDNF and increased oxidative stress may underlie cognitive deficits.
- These findings highlight the critical role of maternal diet in offspring neurodevelopment.
Abstract:
Maternal obesity may affect the child's long-term development and health, increasing the risk of diabetes and metabolic syndrome. In addition to the metabolic and endocrine systems, recent reports have indicated that maternal obesity also modulates neural circuit formation in the offspring. However, this not yet been fully investigated. Here, we examined the effect of diet-induced maternal obesity on hippocampal development and function in the mouse offspring. Adult female mice were fed either a normal diet (ND, 4% fat) or a high-fat diet (HFD, 32% fat) before mating and throughout pregnancy and lactation. After weaning, all offspring were fed with a normal diet. We found that HFD offspring showed increased lipid peroxidation in the hippocampus during early postnatal development. HFD offspring had less brain-derived neurotrophic factor (BDNF) in the hippocampus than ND offspring. BDNF has been shown to play crucial roles in neuronal differentiation, plasticity and hippocampus-dependent cognitive functions such as spatial learning and memory. Using retroviral labeling, we demonstrated that dendritic arborization of new hippocampal neurons was impaired in the young HFD offspring. Finally, we evaluated cognitive function in these offspring using hippocampus-dependent behavioral tasks. The Barnes maze test demonstrated that HFD offspring showed impaired acquisition of spatial learning in the young but not adult period. This study, using a mouse model, indicates that diet-induced maternal obesity impairs hippocampal BDNF production and spatial cognitive function in young offspring, possibly due to their metabolic and oxidative changes.
