Neuroglia in eating disorders (obesity, Prader-Willi syndrome and anorexia nervosa)

The hypothalamus is widely recognized as one of the most extensively studied brain regions involved in the central regulation of energy homeostasis. Within the hypothalamus, peptidergic neurons play a crucial role in monitoring peripheral concentrations of metabolites and hormones, and they finely adjust the sensing of these factors, leading to the activation of either anorexigenic (appetite-suppressing) or orexigenic (appetite-stimulating) pathways. While cortical innervation of the hypothalamus does influence these processes, it is generally considered of secondary importance. Eating-related disorders, such as obesity and anorexia nervosa, are strongly associated with imbalances in energy intake and expenditure. The phenotypes of these disorders can be attributed to dysfunctions in the hypothalamus. Traditionally, it has been believed that hypothalamic dysfunction in these disorders primarily stems from defects in neural pathways. However, recent evidence challenges this perception, highlighting the active participation of neuroglial cells in shaping both physiologic and behavioral characteristics. This review aims to provide an overview of the latest insights into glial biology in three specific eating disorders: obesity, Prader-Willi syndrome, and anorexia. In these disorders, neural dysfunction coincides with glial malfunction, suggesting that neuroglia actively contribute to the development and progression of various neurologic disorders. These findings underscore the importance of glial cells and open up potential new avenues for therapeutic interventions.