Aims: A typical Western diet is excessively fatty, leading to a rapid increase in obesity in human population, including the women of reproductive age. There is growing evidence that maternal high-fat diet (mHFD) increases the risk of neurodevelopmental disorders in the offspring [1, 2, 3]. mHFD affects offspring neurodevelopment through various pathways, including changes in maternal metabolic status, increased chronic inflammation, or alterations in maternal and offspring gut microbiota [4, 5, 6]. Our aim was to evaluate whether mHFD increases maternal chronic inflammation and alters maternal metabolic status and gut microbiota, leading to the changes of offspring gut microbiota and abnormal offspring behavior.
Methods: Female C57B1/6J mice were fed a control diet (CD, 10% fat) or high-fat diet (HFD, 60%) from weaning to lactation. Before mating, the metabolic status of the dams was evaluated by the body mass as well as glucose and insulin tolerance tests. The offspring were weaned to CD. After lactation, the concentration of maternal plasma insulin and proinflammatory cytokines were measured by ELISA tests. We investigated the behavioral phenotype of the offspring in three-chamber sociability, reciprocal social interaction, open field, marble burying, novel object recognition, and Barnes maze tests. To investigate gut microbiota, dam and offspring cecums were collected. Bacterial communities were determined by 16S rRNA amplicon sequencing.
Results: We determined that the consumption of HFD caused metabolic dysfunction but did not increase inflammation in the dams. mHFD changed the relative abundance of different gut bacteria genera in both dams and offspring. Decreased sociability was determined in both mHFD males and females although only males showed increased activity and only females showed decreased repetitive behavior.
Conclusions: Our findings demonstrated, that mHFD altered the composition of the offspring gut microbiota which may contribute to abnormal behavior in a sex-specific manner.