The gut with its considerable surface area, significant microbial mass and recognised associations with immune and neuroendocrine tissues is much more than just a surface for nutrient absorption. In this context, the contribution of the gut to the development of obesity deserves further attention. Among the many functions of the intestinal microbiota, microbial fermentation of otherwise nondigestible fibres provides an additional source of absorbable of energy to the host (up to 10% of daily energy intake has been suggested) and is therefore particularly relevant in the context of obesity. Changes in the gut microbiota reported in human studies of excess body mass include reduced overall microbial diversity and differences in the abundance of key phyla, however variability in results between studies is acknowledged. That said, microbial transfer studies in animal models further support a causative role of the gut microbiota in obesity; transfer of microbiota from obese sources to lean animals results in the development of an obese phenotype in recipient animals. Beyond issues of energy harvest, the potential for the gut microbiota to contribute to the regulation of both satiety, via enteroendocrine pathways, and intestinal permeability, via promotion of a healthy gut mucosa, has also been documented. These pathways extend the role of the gut to beyond just contributing to development of obesity and implicate gut-derived factors in also underpinning risk for obesity-associated disease.