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Maternal palmitoleic acid supplementation attenuates neurodegenerative programming in aged offspring exposed to
Ritsuko Kawaharada1, Reiko Kimura1, Eri Miyata2
1Department of Food and Nutrition, Takasaki University Graduate School of Health and Welfare, 37-1, Nakaorui-machi, Takasaki 370-0033, Gunma, Japan.
Insights
Maternal hyperglycemia may cause lasting brain changes and cognitive issues in offspring. Palmitoleic acid supplementation shows potential to mitigate these adverse effects on brain aging.
Area of Science:
- Neuroscience
- Developmental Biology
- Endocrinology
Background:
- Maternal hyperglycemia is linked to poor neurodevelopment in offspring.
- Long-term impacts of maternal hyperglycemia on offspring brain aging are not well understood.
Purpose of the Study:
- To determine if maternal hyperglycemia causes persistent molecular and behavioral changes in aged male offspring.
- To investigate the protective effects of maternal palmitoleic acid supplementation.
Main Methods:
- Pregnant rats were divided into four groups: control (PCM), diabetic (PDM), diabetic supplemented with conjugated palmitoleic acid (PDM/CPA), and diabetic supplemented with triacylglycerol palmitoleic acid (PDM/TPA).
- Male offspring were assessed at 48 weeks of age for molecular and behavioral alterations.
Main Results:
- Maternal hyperglycemia increased cerebral RAGE and tau phosphorylation, reduced Akt phosphorylation, impaired antioxidant responses (Nrf2), and elevated inflammatory gene expression.
- These molecular changes correlated with impaired recognition memory in offspring.
- Maternal palmitoleic acid supplementation (CPA/TPA) partially reversed these abnormalities.
Conclusions:
- Maternal hyperglycemia can induce persistent neuroinflammation, impaired insulin signaling, and cognitive deficits in aged offspring.
- Palmitoleic acid supplementation may offer partial protection against the detrimental effects of intrauterine hyperglycemic exposure on offspring brain development and aging.
Abstract:
Background/Objectives: Maternal hyperglycemia is associated with adverse neurodevelopmental outcomes in offspring; however, its long-term effects on brain aging remain unclear. This study investigated whether maternal hyperglycemia induces persistent molecular and behavioral alterations in aged male offspring and whether maternal palmitoleic acid supplementation exerts protective effects. Methods: The pregnant rats were divided into four groups: PCM, PDM, PDM/CPA, and PDM/TPA. Male offspring were analyzed at 48 weeks of age. Results: Maternal hyperglycemia significantly increased cerebral RAGE expression (~1.6-fold) and tau phosphorylation (~1.8-fold), accompanied by reduced Akt phosphorylation, impaired Nrf2-related antioxidant responses, and increased inflammatory gene expression. These molecular alterations are associated with impaired recognition memory, as reflected by a marked reduction in the discrimination index in the novel object recognition test. Maternal CPA/TPA supplementation partially attenuated these abnormalities. Conclusions: These findings suggest that maternal hyperglycemia may induce long-lasting molecular alterations associated with neuroinflammation, impaired insulin-related signaling, and cognitive dysfunction in aged offspring. Maternal palmitoleic acid supplementation may partially mitigate the adverse developmental alterations associated with intrauterine hyperglycemic exposure.
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