부산대학교 도서관

Obesity is a global health problem, and the number of reproductive-age women with obesity continues to increase. Cases of maternal obesity induced by a high-fat diet (HFD) have increased in recent years. Different studies have described that maternal HFD can affect the normal development of several organs, making offspring more susceptible to certain diseases. Animal obesity models suggest that a maternal HFD during gestation is a risk factor for developing physiological and behavioural dysfunctions in offspring. We test the hypothesis in mice that maternal HFD without obesity, during pregnancy and lactation, changes the cortical and hippocampal structure and cellular organisation and modifies metabolic-related parameters, and neurogenesis in the adult hippocampus. Female mice were fed different diets from conception: normal fat diet (NFD), HFD throughout gestation and lactation (HFD) or embryonic HFD (Emb-HFD: HFD for 3 days, NFD thereafter). After weaning, the offspring were maintained on NFD. Our data showed that the HFD and Emb-HFD groups developed metabolic disturbances in adulthood and had a greater density of astrocytes and microglia cells, in the cortex and hippocampus. Similarly, we observed that the offspring of mother fed a HFD had a higher density of new-born neurons and a reduced density of mature neurons in the dentate gyrus, indicating that exposure to a maternal HFD can generate changes in adult neurogenesis. In many cases we observed a graded response (NFD < Emb-HFD < HFD) suggesting a very early induction of diet-induced responses, well before any neural differentiation, with exacerbated effects upon continued HFD challenge. This suggests that not only diet during pregnancy is crucial for proper glial cell density and neurogenesis, but also the time of exposure is critical to determine the size of the effects in the offspring brain, caused by maternal HFD.