Food intake not only provides pleasure through exteroceptive sensations such as taste and smell but also elicits beneficial physiological effects via interoceptive signals arising from the gastrointestinal tract and beyond. Among these interoceptive pathways, vagal sensory (vagal afferent) nerves play a central role in transmitting food-derived information to the brain. This review first outlines the anatomical and functional characteristics of vagal sensory nerves. It then examines how food-related signals, including mechanical stretching of the gastrointestinal wall, gastrointestinal and pancreatic hormones such as glucagon-like peptide-1, and microbial metabolites like short-chain fatty acids, are detected by vagal pathways. These inputs collectively regulate food intake, nutrient preferences, and systemic metabolism. Recent studies further suggest that vagal sensory nerves enable the brain to anticipate and adapt to the metabolic demands of food intake, serving as a key mechanism for maintaining homeostasis during rapid postprandial changes. Understanding the role of vagal afferents in sensing meal-derived signals and mediating gut-brain communication provides insights into how interoceptive pathways orchestrate energy balance and hold promise for developing therapeutic strategies for metabolic disorders such as obesity and diabetes. Among these interoceptive pathways, vagal sensory (vagal afferent) nerves play a central role in transmitting food‐derived information to the brain. This review first outlines the anatomical and functional characteristics of vagal sensory nerves. It then examines how food‐related signals, including mechanical stretching of the gastrointestinal wall, gastrointestinal and pancreatic hormones such as glucagon‐like peptide‐1, and microbial metabolites like short‐chain fatty acids, are detected by vagal pathways. These inputs collectively regulate food intake, nutrient preferences, and systemic metabolism. Recent studies further suggest that vagal sensory nerves enable the brain to anticipate and adapt to the metabolic demands of food intake, serving as a key mechanism for maintaining homeostasis during rapid postprandial changes. Understanding the role of vagal afferents in sensing meal‐derived signals and mediating gut–brain communication provides insights into how interoceptive pathways orchestrate energy balance and hold promise for developing therapeutic strategies for metabolic disorders such as obesity and diabetes. In parallel, growing evidence indicates that food ingestion also activates interoceptive pathways: mechanical and chemical stimuli generated as food passes through the gastrointestinal (GI) tract are transmitted subconsciously to the brain. These signals modulate key meal‐related physiological responses, including appetite regulation, reward processing, and glucose metabolism in anticipation of nutrient absorption. Central to this interoceptive sensing are vagal sensory nerves, which convey visceral information from the gut to the brain. FIGURE 2 Vagal afferent nerves linking the gastrointestinal tract to the brain. Vagal nerve terminals innervating the gastrointestinal tract are distributed within the mucosa (mucosal afferents), the myenteric plexus between muscle layers (intraganglionic laminar endings; IGLEs), the longitudinal and circular muscle layers (intramuscular arrays; IMAs), and around or within pancreatic islets (Makhmutova et al., 2021 ). Mechanical stimuli Food intake induces distension of the stomach and intestines, and this mechanical stimulation—specifically the tension and stretch of the gastrointestinal wall—serves as a critical signal to promote meal termination (Phillips & Powley, 1996 ). However, it has long been recognized that gastric distension alone is insufficient to induce a true sense of satiety (Deutsch & Gonzalez, 1980 ; Ritter, 2004 ). Notably, up to 40% of ingested food may have already passed beyond the duodenum by the time individuals perceive fullness and terminate eating (Kaplan et al., 1992 ). Disruption of neural pathways connecting lipid‐responsive vagal afferents to their central projection site in the NTS abolishes lipid preference (Li et al., 2022 ). Specific vagal sensory neurons are activated when lipids reach the intestine, Diet composition profoundly influences the gut microbiota, which, in turn, modulates host physiology through the gut–brain axis. Emerging evidence suggests that vagal sensory pathways are involved in various microbiota‐mediated effects, such as the improvement of autism‐related behaviors and the worsening of mental functions during intestinal inflammation (Chen et al., 2025 ; Sgritta et al., 2019 ). γ‐Aminobutyric acid (GABA), a functional amino acid found in vegetables and fermented foods, is best known as an inhibitory neurotransmitter in the central nervous system. This enhanced vagal activation amplified the satiation induced by the meal alone (Nakamura et al., 2022 ). These findings raise the possibility that the brain‐related benefits of dietary GABA may, at least in part, result from its ability to potentiate meal‐induced vagal activation. In addition, low‐osmolarity stimulation through water intake has been linked to drinking behavior via vagal sensory pathways (Ichiki et al., 2022 ). Intestinal perfusion of water activates a distinct population of vagal sensory neurons, which originate from the common hepatic branch of the vagus nerve. In animal studies, particularly in rat models, the anti‐obesity effects of taVNS have also been reported (Li et al., 2015 ). 5. CONCLUSION Vagal sensory nerves play a critical role in relaying information about ingested food to the brain as subconscious sensory signals. These signals trigger a wide array of physiological responses. Eating is a fundamental behavior necessary for acquiring energy to sustain life. However, the rapid metabolic changes that follow food intake can also be perceived by the body as a form of stress.