Overeating cuts the brain's natural brakes on food intake. This, in turn, would result in neurological changes that continue to fuel unhealthy eating and would lead to obesity, reveals a study in mice.
The results demonstrate how diet-induced obesity alters the function of a crucial neurological feeding suppression system - findings that could help identify novel therapeutic targets for eating disorders and obesity in humans.
‘Researchers found neurons to be highly and uniquely modified in mice who are on a high-fat, obesogenic diet, that eventually lead to a disruption of the natural feeding suppression system of the brain.’
Obesity, a disease that affects more than 500 million adults worldwide and is a large factor in the increased incidence of a myriad of other serious health issues, is often considered to be one of the most pressing global health concerns. While obesity can be linked to a few, rarely occurring medical causes, unhealthy eating habits are widely recognized as the largest determinant. However, little is known about how obesity impacts the brain or underlying neurological mechanisms, to contribute to these adverse eating behaviors.
Previous research suggests that the lateral hypothalamic area (LHA), a brain region that mediates physiological functions related to survival, plays a crucial role in controlling eating behavior. In a mouse model of obesity, Mark Rossi and colleagues used a combination of single-cell RNA sequencing and two-photon calcium imaging to identify obesity-related alterations in particular cells within the LHA. The results identified a discrete class of cells - glutamatergic neurons - that functionally put the brakes on feeding to suppress food intake beyond satiation, in ideal conditions. However, in mice fed high-fat, obesogenic diets, Rossi et al. found these neurons to be highly and uniquely modified in a way that disrupted this natural feeding suppression system to promote overeating and obesity. In a related Perspective, Stephanie Borgland discusses the study in more detail.