Gut microbiota as a novel therapeutic target for eating disorders and obesity

Abstract

The gut–brain axis constitutes a bidirectional communication network linking the intestinal microbiota and the central nervous system. Through this communication axis, the gut microbiota exerts a major influence on food intake under physiological and pathophysiological conditions. Exposure to a Western diet has been associated with dysbiosis of the gut microbiota, leading to profound changes in the gut–brain axis and promoting compulsive-like eating patterns. Alterations in the gut microbiota influence brain activity via multiple routes, including activation of vagal afferents, modulation of systemic immune and endocrine responses, and the action of microbiota-derived metabolites. Through these mechanisms, gut microbiota imbalance alters metabolic and reward-related brain processes that govern eating behaviour. Thus, gut microbiota interacts with homeostatic pathways by modulating satiety-related hypothalamic mechanisms, thereby influencing appetite and energy balance. In parallel, microbiota-dependent signalling affects hedonic feeding by shaping mesolimbic dopamine activity. Neuroinflammation is another key mechanistic interface within the gut microbiota–brain axis contributing to the development of metabolic disorders. Gut microbiota dysbiosis can increase intestinal permeability, facilitating the translocation of microbial components that promote systemic inflammation. Given this convergence between metabolic, inflammatory and reward mechanisms, modulation of the gut microbiota has emerged as a potential therapeutic approach for obesity and eating disorders. Prebiotics, probiotics, postbiotics, synbiotics and faecal microbiota transplantation are currently under investigation for their capacity to restore microbial balance and improve these metabolic and behavioural disorders. This review primarily focuses on the neurobehavioural regulation of feeding and its dysregulation, with particular emphasis on gut–brain axis mechanisms.