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Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes
Published on: June 28, 2024
Maternal High-fat Diet Programs Offspring Emotional Behavior in Adulthood
Gudrun Winther1, Betina Elfving1, Heidi Kaastrup Müller1
1Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Risskov DK-8240, Denmark.
Maternal high-fat diet (HFD) exposure in rats induced anxiety-like behaviors in offspring. This was linked to increased hippocampal neuroinflammation and altered stress hormone pathways, suggesting a molecular basis for prenatal HFD effects.
Area of Science:
- Neuroscience
- Developmental Biology
- Endocrinology
Background:
- Prenatal exposure to high-fat diets (HFD) is linked to metabolic and mental health issues in offspring.
- The molecular mechanisms, particularly neuroinflammation and stress axis regulation, are not fully understood.
Purpose of the Study:
- To investigate the impact of maternal HFD on offspring's anxiety, depression, and memory.
- To identify biomarkers in the hippocampus related to neuroinflammation and stress responses.
Main Methods:
- Female Sprague-Dawley rats were fed a control or HFD before and during gestation/lactation.
- Offspring behavior was assessed using elevated plus maze, forced swim test, novel object recognition, and open field tests.
- Hippocampal gene expression of inflammatory markers (TNF-α, MCP-1) and stress-related genes (CRHR2, KMO, KAT1) was quantified via real-time qPCR.
Main Results:
- Maternal HFD induced anxiety-like behaviors in offspring, irrespective of sex.
- Increased hippocampal mRNA levels of tumor necrosis factor-alpha (TNF-α) and monocyte-chemoattractant protein-1 (MCP-1) were observed.
- Elevated corticosteroid releasing hormone receptor 2 (CRHR2) and kynurenine monooxygenase (KMO) mRNA, with decreased kynurenine aminotransferase I (KAT1) mRNA, were found in offspring hippocampi.
Conclusions:
- Maternal HFD exposure can lead to anxiety-like behaviors in offspring.
- Hippocampal neuroinflammation and altered stress axis gene expression are potential biological mechanisms underlying these effects.
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