Gut microbiota may shape eating behavior and guide new obesity treatments

By Tarun Sai LomteReviewed by Susha Cheriyedath, M.Sc.Jul 12 2026

From appetite signals to food reward, researchers reveal how gut microbes may influence disordered eating and obesity, while highlighting the evidence still needed before microbiota-based therapies reach clinical practice.

Study: Gut microbiota as a novel therapeutic target for eating disorders and obesity. Image Credit: Shutterstock AI / Shutterstock

In a recent review published in the British Journal of Pharmacology, researchers examined the neurobehavioral regulation and dysregulation of feeding, focusing on mechanisms of the gut-brain axis and microbiota-targeted interventions.

Obesity and eating disorders are increasingly prevalent worldwide. While both share common physiological, neurobiological, and behavioral mechanisms, they have distinct phenotypic manifestations and underlying mechanisms. As such, understanding their distinct and shared mechanisms is necessary to identify common treatment targets. In this review, researchers summarized the neurobehavioral mechanisms underlying feeding regulation and dysregulation.

Physiological Regulation and Dysregulation of Food Intake

The physiological regulation of food intake hinges on the interactions between the reward-driven hedonic and energy-balance-driven homeostatic neural systems; their disruption is a key underlying mechanism of eating disorders and obesity. Short-term gut-derived signals, including ghrelin, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY), and long-term adiposity signals, such as leptin, converge with brainstem and hypothalamic circuits in regulating meal timing, size, and energy homeostasis.

The dorsomedial nucleus integrates metabolic and circadian signals, and its functional disruption has been linked to obesity and hyperphagia. In addition, hedonic control plays a significant role in regulating food intake, shaped by environmental cues and palatability. The prefrontal cortex (PFC) underlies voluntary, conscious eating decisions, and its dysfunction may weaken executive control and contribute to compulsive and impulsive behaviors associated with obesity and eating disorders.

Further, the mesolimbic dopamine system, which encodes the pleasurable and motivational aspects of food, overlaps with neural circuits engaged by addictive drugs. These regions have receptors for ghrelin, GLP-1, insulin, leptin, and orexin, enabling neuropeptides and metabolic hormones to modulate reward processing and couple energy status to food seeking.

Food intake dysregulation is the persistent disruption in mechanisms regulating satiety, hunger, and their relationships with food. This change could be restriction, excessive consumption, recurrent overeating, or loss of eating control, with some patterns, particularly recurrent overeating and compulsive intake, contributing to overweight and obesity. Binge-eating disorder involves recurrent binge-eating episodes, while bulimia nervosa also involves compensatory behaviors intended to prevent weight gain. Other eating disorders, e.g., anorexia nervosa, are associated with severe self-imposed restriction, sometimes accompanied by purging.

Gut-Brain Axis and Dysbiosis

The gut-brain axis is a bidirectional communication network that links the central nervous system (CNS) and the intestinal microbiota, primarily through neural, metabolic, immune, and endocrine pathways. Microbiota-derived metabolites, especially short-chain fatty acids, play a major role in regulating neuroinflammatory processes, glial and neuronal activity, and in maintaining the integrity of the blood-brain barrier.

Evidence suggests that the gut microbiota has an important role in modulating reward and homeostatic systems in the CNS and maintaining balance between appetite-suppressing and appetite-stimulating signals in the adipose tissue and gut. The disruption of this balance may contribute to the development or persistence of obesity and some eating-related disorders. The composition of the gut microbiota can modify hedonic and homeostatic control of food intake, and diet- or stress-associated dysbiosis may promote excessive intake of palatable foods, particularly in experimental models.

Studies have linked obesity to increased intestinal permeability, impaired motility, and metabolic endotoxemia, characterized by elevated levels of circulating microbial products that promote inflammation, as well as chronic low-grade inflammation, processes that have been associated with dysbiosis. Dysbiosis-related mucin layer degradation and tight junction protein downregulation facilitate the interaction of bacterial lipopolysaccharide (LPS) and other components with toll-like receptors (TLRs), stimulating immune responses.

LPS has been reported to modulate food-seeking behavior via toll-like receptor 4 (TLR4) signaling in the reward system, primarily in experimental studies. Further, elevated epithelial permeability facilitates the translocation of bacterial components into the circulation, inducing metabolic endotoxemia and low-grade inflammation. Bacterial components and inflammatory molecules may alter blood-brain barrier integrity and promote neuroinflammatory signaling, thereby affecting both hedonic and homeostatic centers. These interactions may create a bidirectional cycle in which diet, stress, and disrupted eating patterns alter the microbiota, while dysbiosis reinforces metabolic and behavioral disturbances that encourage further unhealthy intake.

Potential Gut Microbiota-Based Therapeutic Approaches

Gut microbiota-based interventions represent potential strategies for the prevention and treatment of obesity and related conditions. Prebiotics are substrates selectively used by microbes and confer health benefits to the host. In one small clinical study, resistant starch was associated with lower body weight, attenuated systemic inflammation, and improved glucose tolerance and lipid profile in adults with overweight or obesity.

Probiotics are live microbes that confer health benefits when consumed in adequate amounts. Various trials have investigated the use of probiotics to mitigate obesity. Small clinical trials of specific strains and formulations, including Akkermansia muciniphila, Bifidobacterium lactis, and Lactiplantibacillus plantarum, have reported improvements in selected obesity-related metabolic parameters and weight-related outcomes. Synbiotics are a combination of probiotics and prebiotics, and some studies suggest that particular formulations may offer greater benefits than either component alone.

In mice, the combination of galactooligosaccharides and L. plantarum LLY-606 increased energy expenditure and reduced hepatic lipid accumulation. In humans, a combination of fructooligosaccharides with Streptococcus thermophilus and several strains of Bifidobacterium and Lactobacillus has been reported to result in fat mass loss and changes in homeostatic feeding, such as increased fullness and decreased desire to eat. However, these findings come from individual studies and require confirmation in larger controlled trials. Preliminary research has also examined probiotics for stress, depressed mood, emotional eating, and food cravings associated with eating disorders, but these findings do not establish that probiotics can treat an eating disorder.

Postbiotics and fecal microbiota transplantation (FMT) have also been explored. Human trials of FMT have generally altered gut microbial composition without consistently improving body weight or metabolic outcomes, whereas stronger weight-related effects have been observed in animal models. Safety, donor selection, standardization, and the durability of microbial changes also remain important concerns.

Concluding Remarks

Taken together, the role of the gut microbiota in obesity and food intake regulation has been increasingly recognized in recent years. However, this has not yet translated into validated biomarkers or broadly effective clinical interventions, warranting sustained efforts. Microbiota-targeted therapies are not established treatments; much of the mechanistic evidence comes from animal models, and human studies are generally small, short, and heterogeneous.

Identifying gut microbiota-based biomarkers and novel therapeutic targets for obesity and related disorders remains challenging because microbial signatures can vary with diet, medication use, age, geography, and analytical methods. Reliable biomarkers may require standardized, longitudinal, multi-omic studies that integrate microbial composition and function with metabolites and host factors.