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Life sciences · Review
Nutrients · October 5, 2026
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Visceral adipose tissue (VAT) dysfunction is a major determinant of obesity-related metabolic disorders, including insulin resistance, metabolic syndrome, cardiovascular disease, and chronic low-grade inflammation. Growing evidence indicates that VAT function is regulated by a complex interplay between nutrition, circadian rhythms, intestinal melatonin secretion, and the gut microbiota rather than by isolated metabolic pathways. The gastrointestinal tract represents an important interface between dietary exposures, microbial activity, immune signaling, and host metabolic regulation. Melatonin is a potential component of this network because it participates in circadian regulation and has been detected in gastrointestinal tissues, while experimental studies suggest that intestinal melatonin signaling may interact with gut microbial and metabolic processes. However, the cellular sources, quantitative contribution, local dynamics, and physiological significance of intestinal melatonin remain incompletely established, particularly in humans. This narrative review integrates current evidence regarding the interactions between nutrition, circadian regulation, intestinal melatonin, gut microbiota, and visceral adipose tissue. Rather than proposing a validated causal pathway, we introduce the Gut–Melatonin–Visceral Adipose Tissue (Gut–Melatonin–VAT) Axis as an integrative, hypothesis-generating conceptual framework that organizes established interactions together with candidate mechanisms requiring further experimental validation. Particular attention is given to the bidirectional relationships among dietary composition, meal timing, microbial rhythmicity, intestinal signaling, immune regulation, and VAT dysfunction. The framework may provide a basis for generating testable hypotheses concerning nutritional, chrononutritional, microbiota-targeted, and melatonin-related interventions, while recognizing that direct human evidence validating the complete pathway is currently lacking.