The microbiota-nutrition relationship is undoubtedly one of the most visible areas of human-microbe mutualism. The intestinal microbiota metabolizes food ingested by the host, as well as host elements (mucins). Conversely, products of microbial metabolism can be converted by the host. The profile of metabolites present in the gut therefore depends on the combination of the host's eukaryotic metabolism and the microbiota's prokaryotic metabolism.
Significant differences are observed in the products of intestinal metabolism in axenic mice, compared with conventional mice. Antibiotic administration can have an effect not only on the metabolic profile of the gut, but also on the systemic metabolic profile of the treated animal. Treatment of mice with streptomycin affects the levels of 87% of identified metabolites in feces. Important metabolic pathways such as the metabolism of bile salts, pro-inflammatory lipids and steroid hormones are affected. These effects are not confined to the stool. Treatment of rats with a combination of penicillin and streptomycin results in changes in metabolite profiles not only in the stool, but also in the urine, indicating a systemic effect.
Axenic mice have reduced adiposity and require an increased diet to reach the same weight as conventional mice. They have a reduced capacity to extract energy from a diet rich in carbohydrates. They are resistant to a Western-style diet, rich in fats and sucrose and virtually free of carbohydrates. Compared with conventional mice, the small intestine of axenic mice shows higher expression of angiopoietin-like protein 4 (ANGPTL4) or fasting-induced adipose factor (FIAF), which induces fatty acid oxidation in skeletal muscle. The intestinal microbiota therefore appears capable of directly modulating host metabolism, particularly lipid metabolism.
