Obesity is a worldwide epidemiologic syndrome characterized by fat mass accumulation, mainly visceral fat. Current thinking considers a potential role of gut microbiota on the development of obesity and its related comorbidities. Gut microbiota can influence energy extraction from food, lipid metabolism, immune response and endocrine functions and its profile has shown to differs between obese and lean subjects. This short revision resumes the main findings that contributed to build the current background linking changes in gut microbiota profile with obesity and obesityrelated comorbidities and the potential role of gut microbiota modulation to treat these metabolic disturbances.

In recent decades, experimental and clinical studies have associated the development of obesity with the composition of the gut microbiota. Mechanisms potentially involved in the contribution of gut microbiota to body weight gain include changes in energy extraction from the diet and the modulation of lipid metabolism, endocrine functions, and the immune system. The host's specific genetic heritage, the type and amount of food intake, chronic inflammation, reduced body energy expenditure, and exposure to obesogenic pollutants are also potential contributing factors. The pathophysiological processes involved in the relationship between gut microbiota and obesity are not fully understood, and further studies are needed to establish whether differences in gut bacterial diversity between obese and normal body weight individuals are the cause or a consequence of obesity.

ObjectiveTo describe the protocol of the SURgically induced Metabolic effects on the Human GastroIntestinal Tract (SURMetaGIT) study, a clinical pan-omics study exploring the gastrointestinal tract as a central organ driving remission of type 2 diabetes mellitus (T2DM) after Roux-en-Y gastric bypass (RYGB). The main points considered in the study’s design and challenges faced in its application are detailed.MethodsThis observational, longitudinal, prospective study involved collection of gastrointestinal biopsy specimens, faeces, urine, and blood from 25 obese women with T2DM who were candidates for RYGB (20 patients for omics assessment and 5 for omics validation). These collections were performed preoperatively and 3 and 24 months postoperatively. Gastrointestinal transcriptomics; faecal metagenomics and metabolomics; plasma proteomics, lipidomics, and metabolomics; and biochemical, nutritional, and metabolic data were assessed to identify their short- and long-term correlations with T2DM remission.ResultsData were collected from 20 patients before and 3 months after RYGB. These patients have nearly completed the 2-year follow-up assessments. The five additional patients are currently being selected for omics data validation.ConclusionThe multi-integrated pan-omics approach of the SURMetaGIT study enables integrated analysis of data that will contribute to the understanding of molecular mechanisms involved in T2DM remission after RYGB.

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