The development of metabolic diseases is linked to the gut microbiota. A cross-sectional study involving 45 children (6 to 12 years old) was conducted to investigate the relationship between gut microbiota and childhood obesity. Anthropometric and metabolic measurements, food-frequency questionnaires (FFQs), and feces samples were obtained. Using the body mass index (BMI) z-score, we categorized each participant as normal weight (NW), or overweight and obese (OWOB). We determined 2 dietary profiles: one with complex carbohydrates and proteins (pattern 1), and the other with saturated fat and simple carbohydrates (pattern 2). The microbial taxonomic diversity and metabolic capacity were determined using shotgun metagenomics. We found differences between both BMI groups diversity. Taxa contributing to this difference, included Eubacterium sp., Faecalibacterium prausnitzii, Dialister, Monoglobus pectinilyticus, Bifidobacterium pseudocatenulatum, Intestinibacter bartlettii, Bacteroides intestinalis, Bacteroides uniformis, and Methanobrevibacter smithii. Metabolic capacity differences found between NW and OWOB, included the amino acid biosynthesis pathway, the cofactor, carrier, and vitamin biosynthesis pathway, the nucleoside and nucleotide biosynthesis and degradation pathways, the carbohydrate-sugar degradation pathway, and the amine and polyamine biosynthesis pathway. We found significant associations between taxa such as Ruminococcus, Mitsuokella multacida, Klebsiella variicola, and Citrobacter spp., metabolic pathways with the anthropometric, metabolic, and dietary data. We also found the microbiome's lipooligosaccharide (LOS) category as differentially abundant between BMI groups. Metabolic variations emerge during childhood as a result of complex nutritional and microbial interactions, which should be explained in order to prevent metabolic illnesses in adolescence and maturity. IMPORTANCE The alteration of gut microbiome composition has been commonly observed in diseases involving inflammation, such as obesity and metabolic impairment. Inflammatory host response in the gut can be a consequence of dietary driven dysbiosis. This response is conducive to blooms of particular bacterial species, adequate to survive in an inflammatory environment by means of genetical capability of utilizing alternative nutrients. Understanding the genomic and metabolic contribution of microbiota to inflammation, including virulence factor prevalence and functional potential, will contribute to identifying modifiable early life exposures and preventive strategies associated with obesity risk in childhood.

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