Irritable bowel syndrome: a new therapeutic target when treating obesity?

There is accumulating evidence showing that obesity is due not merely to increased food intake, but could have a more complex pathophysiology possibly originating from the gut. Due to its microbiological, hormonal, and nutritional aspects, the gut could represent a starting point for the treatment of weight excess. Obesity is associated with a change of microbiota composition that not only could increase the calorie extraction from food but also could create a functional derangement resulting in irritable bowel syndrome (IBS). Several mechanisms have been postulated to explain this association, such as specific foods that are poorly absorbed, i.e., carbohydrates and lipids, as well as conditions of psychological stress which could stimulate colonic hypersensitivity giving rise to IBS symptoms. Another factor involved in this link could be the subclinical inflammation typical of obesity, characterized by the release of inflammatory mediators that can irritate intestinal nerve endings. The change of levels of some anorexigenic hormones, as well as the alterations of the gut microbiota with the reduction of the bacteroides/Firmicutes ratio, could also contribute to the pathogenesis of IBS related to obesity. Thus, the aim of this manuscript is to review the current evidence on the association between obesity and IBS while providing physiopathological hypotheses that may explain this link. Further, we will report the effect of weight loss on IBS symptoms, highlighting the importance of an accurate assessment of gut function in obese patients.