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Diet-induced obesity in female mice leads to peroxidized lipid accumulations and impairment of hippocampal neurogenesis during the early life of their offspring

Yusuke Tozuka^*,,, Etsuko Wada^*, and Keiji Wada^*,,1

^* Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan;

Japan Association for the Advancement of Medical Equipment, Tokyo, Japan; and

Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama, Japan

¹Correspondence: Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigasi, Kodaira, Tokyo 187-8502, Japan. E-mail: wada{at}ncnp.go.jp

Maternal obesity may affect the child’s long-term development and health. However, there is little information about the involvement of maternal obesity in the brain development of offspring. Here, we investigated the effects of maternal obesity on the hippocampal formation of offspring. Adult female mice were fed either a normal diet (ND, 4% fat) or a high-fat diet (HFD, 32% fat) 6 wk before mating and throughout pregnancy and the majority of lactation. We found that infants from HFD-fed dams (HFD offspring) showed obesity and hyperlipidemia during suckling. In HFD offspring, lipid peroxidation was promoted in serum and the hippocampal dentate gyrus, where neurogenesis takes place throughout postnatal life. Using a BrdU-pulse labeling study, we showed that malondialdehyde, a product of peroxidized lipids, reduced the proliferation of hippocampal progenitor cells in vitro and that neurogenesis in HFD offspring during postnatal development was similarly lowered relative to the ND animals. These results indicated that maternal obesity impairs hippocampal progenitor cell division and neuronal production in young offspring possibly due to metabolic and oxidative changes.—Tozuka, Y., Wada, E., Wada, K. Diet-induced obesity in female mice leads to peroxidized lipid accumulations and impairment of hippocampal neurogenesis during the early life of their offspring.

Key Words: lactation • neural progenitor cells • hight-fat diet • metabolic abnormalities • oxidative stress • brain development

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