Maternal high-fat diet prevents developmental programming by early-life stress
Open accessAbstract
Anxiety disorders and depression are well-documented in subjects exposed to adverse childhood events. Recently, maternal obesity and/or maternal consumption of high-fat diets (HFD) have been also proposed as risk factors for offspring mental health. Here using an animal model in rats, we explored the combinatorial effects of a maternal HFD (40% of energy from fat without impact on maternal weight; during gestation and lactation) and maternal separation (MS) in offspring. In the prefrontal cortex (PFC) of pups, MS led to changes in the expression of several genes such as Bdnf(brain derived neurotrophic factor),5HT-r1a(serotonin receptor 1a) and Rest4(neuron-restrictive silencer element, repressor element 1, silencing transcription factor (Rest), splicing variant 4). Surprisingly, perinatal HFD strongly attenuated the developmental alterations induced by MS. Furthermore, maternal HFD totally prevented the endophenotypes (anxiety, spatial memory, social behavior, hypothalamic–pituitary–adrenal (HPA) axis response to stress, hippocampal neurogenesis and visceral pain) associated with MS at adulthood. Finally, we also demonstrated that HFD intake reduced anxiety and enhanced maternal care in stressed dams. Overall, our data suggest that a HFD restricted to gestation and lactation, which did not lead to overweight in dams, had limited effects in unstressed offspring, highlighting the role of maternal obesity, rather than fat exposure per se,on brain vulnerability during development.
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Particular consumption of high-fat and/or high-sugar during pregnancy, childhood and adolescence can result in structural changes in the PFC and deficits in executive functioning.
“Particular consumption of high-fat and/or high-sugar during pregnancy, childhood and adolescence can result in structural changes in the PFC and deficits in executive functioning [308–311].”
From Development of prefrontal cortex (2022) · cites this paper as [311]
The Introduction reports that maternal obesity or high-fat diets may affect offspring brain function and have been associated with spatial-learning deficits. It does not attribute structural PFC changes or executive-function deficits to diet, or address high-sugar consumption and diet during childhood or adolescence. The Discussion also reports that the study's maternal high-fat diet had little adverse effect on offspring and attenuated effects of early-life stress. (LLM, conf=0.84)
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- Authors
- Rincel, M., Lépinay, A. L., Delage, P., Fioramonti, J., Théodorou, V. S., Layé, S., & Darnaudéry, M.
- Affiliations
- Université de Bordeaux (FR)
- Toxicologie Alimentaire (FR)
- Corresponding author
- Darnaudéry, M
- Venue
- Translational Psychiatry
- Published
- 2016-11-29
- Volume
- 6
- Issue
- 11
- Pages
- e966-e966
- ISSN
- 2158-3188 (ISSN-L)
- PMC
- PMC5290357
- OpenAlex
- W2557377799
- Cited by
- 69
- References
- 70
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 6 · 2023: 5 · 2022: 10 · 2021: 11 · 2020: 8 · 2019: 8 · 2018: 7 · 2017: 3 · 2016: 1
- FWCI
- 7.37
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Translational Psychiatry (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by)
- Oskar-Bordeaux (Universite de Bordeaux) (submittedVersion, cc-by)
- Funders
- Agence Nationale de la Recherche (ANR-12-DSSA-0004, ANR-12)
- Ministère de l'Enseignement Supérieur et de la Recherche
- Université de Bordeaux
- Institut National de la Recherche Agronomique
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Maternal Mental Health During Pregnancy and Postpartum
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- maternal high-fat diet, developmental programming, early life stress, maternal separation, maternal obesity, prefrontal cortex, brain-derived neurotrophic factor, serotonin receptor 1A, anxiety, spatial memory, social behavior, hypothalamic-pituitary-adrenal axis, hippocampal neurogenesis, visceral pain, maternal care, offspring mental health
- MeSH terms
- RE1-Silencing Transcription Factor, Animals, Animals, Newborn, Anxiety, Body Weight, Disease Models, Animal, Female, Life Change Events, Maternal Behavior, Maternal Deprivation, Pregnancy, Prenatal Exposure Delayed Effects, Repressor Proteins, Rats, Wistar, Prefrontal Cortex, Brain-Derived Neurotrophic Factor, Receptor, Serotonin, 5-HT1A, Diet, High-Fat
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