Maternal overnutrition induces long-term cognitive deficits across several generations
Open accessAbstract
Ample evidence from epidemiological studies has linked maternal obesity with metabolic disorders such as obesity, cardiovascular disease, and diabetes in the next generation. Recently, it was also shown that maternal obesity has long-term effects on the progeny's central nervous system. However, very little is known regarding how maternal overnutrition may affect, in particular, the cognitive abilities of the offspring. We reported that first-generation offspring exposed to a maternal high-fat diet (MHFD) displayed age-dependent cognitive deficits. These deficits were associated with attenuations of amino acid levels in the medial prefrontal cortex and the hippocampus regions of MHFD offspring. Here, we tested the hypothesis that MHFD in mice may induce long-term cognitive impairments and neurochemical dysfunctions in the second and third generations. We found that MHFD led to cognitive disabilities and an altered response to a noncompetitive receptor antagonist of the N-Methyl-D-aspartic acid (NMDA) receptor in adult MHFD offspring in both second and third generations in a sex-specific manner. Our results suggest that maternal overnutrition leads to an increased risk of developing obesity in subsequent generations as well as to cognitive impairments, affecting learning and memory processes in adulthood. Furthermore, MHFD exposure may facilitate pathological brain aging which is not a consequence of obesity. Our findings shed light on the long-term effects of maternal overnutrition on the development of the central nervous system and the underlying mechanisms which these traits relate to disease predisposition.
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- Authors
- Sarker, G., & Peleg-Raibstein, D.
- Affiliations
- ETH Zurich (CH)
- Laboratory of Translational Nutrition Biology, The Swiss Federal Institute of Technology, ETH Zürich, Schorenstrasse 16, 8603 Schwerzenbach, Switzerland
- Venue
- Nutrients
- Publisher
- MDPI AG
- Published
- 2018-12-20
- Volume
- 11
- Issue
- 1
- Pages
- 7
- ISSN
- 2072-6643 (ISSN-L)
- PMC
- PMC6356622
- OpenAlex
- W2905480859
- Cited by
- 52
- References
- 80
- Citations by year
- 2026: 1 · 2025: 9 · 2024: 2 · 2023: 4 · 2022: 6 · 2021: 14 · 2020: 10 · 2019: 6
- FWCI
- 8.28
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- Nutrients (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Repository for Publications and Research Data (ETH Zurich) (submittedVersion, cc-by)
- ETH Zürich Research Collection (cc-by)
- Funders
- The Swiss Federal Institute of Technology, ETH Zürich (ETH-15 13-1)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolomics and Mass Spectrometry Studies
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- maternal overnutrition, maternal high-fat diet, transgenerational effects, cognitive impairment, learning and memory, NMDA receptor, amino acid levels, medial prefrontal cortex, hippocampus, brain aging, sex differences, obesity predisposition, central nervous system development
- MeSH terms
- Animals, Cognition, Cognition Disorders, Female, Mice, Inbred C57BL, Pregnancy, Prenatal Exposure Delayed Effects, Receptors, N-Methyl-D-Aspartate, Maternal Exposure, Maternal Nutritional Physiological Phenomena, Overnutrition, Mice, Diet, High-Fat
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