[Introduction]
Obese people are increasing rapidly at a global level. Although obesity markedly increases the risk for the onset of depression, the biological mechanisms that link between depression and obesity remain unclear. Our preliminary findings suggested that stress sensitivity in obese animals may be increased partly due to the decrease in hippocampal neurogenesis, which contributes to the development of depression. We hypothesized that weight-control intervention in obese animals may lead to the decrease in risk of depression. In this study, we investigated the effect of weight-control on hippocampal neurogenesis in high-fat diet induced obese mice.
[Methods]
Male ICR mice (4 weeks old on arrival) were fed a 45% high-fat diet (HFD) for 7 weeks. Subsequently, they are assigned to two groups; weight-controlled group was subjected to diet substitution from HFD to control diet, HFD continuation group was maintained on a HFD. Three weeks after diet substitution, all mice were perfused, brains were removed and coronal sections at 30μm in thickness were cut throughout hippocampus. Every 8th section was processed for doublecortin (DCX) immunostaining and quantified the number of DCX-positive cells in the dentate gyrus.
[Results]
In weight-controlled group, body weight changes were significantly decreased compared with HFD continuation group. There was no significant difference in the number of DCX-positive cells between weight-controlled group and HFD continuation group. However, a significant negative correlation was found between the number of DCX-positive cells and body weight change rate during weight-control intervention for 3 weeks.
[Discussion]
The present findings suggest that the change in hippocampal neurogenesis in obese mice may be dependent on the degree of body weight change. In further study, we need to assess behavioral testing for depression or anxiety after weight-control intervention.