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Perinatal high-fat diet increases hippocampal vulnerability to the adverse effects of subsequent high-fat feeding
Amandine L Lépinay1, Thomas Larrieu1, Corinne Joffre1
1INRA, Nutrition et Neurobiologie Intégrée, UMR 1286, 33000 Bordeaux, France; Université de Bordeaux, Nutrition et Neurobiologie Intégrée, UMR 1286, 33000 Bordeaux, France.
Insights
Maternal high-fat diet (HFD) during pregnancy and lactation sensitizes offspring to later HFD, impairing spatial memory and hippocampal function. Early HFD exposure with later HFD intake negatively impacts cognitive development and neuroplasticity.
Area of Science:
- Neuroscience
- Nutritional Science
- Developmental Biology
Background:
- Maternal high-fat diet (HFD) and altered polyunsaturated fatty acid (PUFA) intake are increasing in women of childbearing age.
- The impact of maternal HFD on offspring cognitive function remains largely unknown.
Purpose of the Study:
- To investigate the long-term effects of perinatal HFD with an unbalanced n-6/n-3 PUFA ratio on hippocampal function in adult rats.
- To explore the combined effects of perinatal HFD and post-weaning HFD exposure on cognitive performance and hippocampal alterations.
Main Methods:
- Dams were fed control or HFD (high lipid, unbalanced n-6/n-3 PUFA ratio) during gestation and lactation.
- Offspring received control or HFD post-weaning.
- Hippocampus-dependent memory was assessed via water-maze task.
- PUFA levels, gene expression, neurogenesis, and astrocyte morphology were analyzed.
Main Results:
- Perinatal HFD induced lasting metabolic changes and some hippocampal gene expression alterations but did not affect memory.
- Offspring exposed to HFD both perinatally and post-weaning showed impaired spatial memory, reduced neurogenesis, altered PUFA levels (low n-3, high n-6), and downregulated plasticity-related genes.
- Exposure to HFD only after weaning did not impair memory, suggesting perinatal HFD sensitizes offspring to later HFD effects.
Conclusions:
- Perinatal exposure to an unbalanced n-6/n-3 PUFA ratio in HFD primes offspring for adverse cognitive and hippocampal outcomes from subsequent HFD.
- Maternal dietary fat composition during critical developmental periods significantly influences long-term offspring brain health and cognitive function.
Abstract:
Epidemiological observations report an increase in fat consumption associated with low intake of n-3 relative to n-6 polyunsaturated fatty acids (PUFAs) in women of childbearing age. However, the impact of these maternal feeding habits on cognitive function in the offspring is unknown. This study aims to investigate the impact of early exposure to a high-fat diet (HFD) with an unbalanced n-6/n-3 PUFAs ratio on hippocampal function in adult rats. Furthermore, we explored the effects of perinatal HFD combined with exposure to HFD after weaning. Dams were fed a control diet (C, 12% of energy from lipids, n-6/n-3 PUFAs ratio: 5) or HFD (HF, 39% of energy from lipids, n-6/n-3 PUFAs ratio: 39) throughout gestation and lactation. At weaning, offspring were placed either on control (C-C, HF-C) or high-fat (HF-HF) diets. In adulthood, hippocampus-dependent memory was assessed using the water-maze task and potential hippocampal alterations were determined by studying PUFA levels, gene expression, neurogenesis and astrocyte morphology. Perinatal HFD induced long-lasting metabolic alterations and some changes in gene expression in the hippocampus, but had no effect on memory. In contrast, spatial memory was impaired in animals exposed to HFD during the perinatal period and maintained on this diet. HF-HF rats also exhibited low n-3 and high n-6 PUFA levels, decreased neurogenesis and downregulated expression of several plasticity-related genes in the hippocampus. To determine the contribution of the perinatal diet to the memory deficits reported in HF-HF animals, an additional experiment was conducted in which rats were only exposed to HFD starting at weaning (C-HF). Interestingly, memory performance in this group was similar to controls. Overall, our results suggest that perinatal exposure to HFD with an unbalanced n-6/n-3 ratio sensitizes the offspring to the adverse effects of subsequent high-fat intake on hippocampal function.
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