This study investigates how dietary fiber influences gut microbial tryptophan metabolism, which can produce beneficial or adverse metabolites. The research uses in vitro cultures and animal experiments to assess the competition for tryptophan among gut microorganisms and the resulting metabolites. Key findings include: 1. **Substrate Availability**: The availability of tryptophan and simple carbohydrates from fiber degradation significantly affects the production of tryptophan metabolites. Higher tryptophan availability promotes the production of beneficial metabolites like indolelactic acid (ILA) and indolepropionic acid (IPA), while inhibiting the production of indole. 2. **Carbohydrate Availability**: Simple carbohydrates, such as those found in pectin, inhibit indole production by repressing the expression of the tnaA gene in *Escherichia coli*. This inhibition allows more tryptophan to be available for other microorganisms, leading to increased production of ILA and IPA. 3. **Fiber Degradation**: *Bacteroides thetaiotaomicron* degrades pectin into monosaccharides, which cross-feed to *E. coli* and inhibit indole production through catabolite repression. This results in increased tryptophan availability for *Clostridium sporogenes*, which produces ILA and IPA. 4. **Human Studies**: In vivo experiments in gnotobiotic mice and human fecal cultures confirmed that dietary fiber reduces indole production while increasing ILA and IPA. This effect is consistent across different microbial communities and dietary fiber types. 5. **Mechanistic Model**: The study proposes a model explaining how dietary fiber interventions can shift gut microbial tryptophan metabolism towards beneficial metabolites. This model emphasizes the role of microbial competition, catabolite repression, and substrate availability in determining the balance between beneficial and potentially adverse metabolites. Overall, the findings provide a rationale for using dietary fiber interventions to promote the production of beneficial tryptophan metabolites and reduce the production of potentially harmful metabolites.This study investigates how dietary fiber influences gut microbial tryptophan metabolism, which can produce beneficial or adverse metabolites. The research uses in vitro cultures and animal experiments to assess the competition for tryptophan among gut microorganisms and the resulting metabolites. Key findings include: 1. **Substrate Availability**: The availability of tryptophan and simple carbohydrates from fiber degradation significantly affects the production of tryptophan metabolites. Higher tryptophan availability promotes the production of beneficial metabolites like indolelactic acid (ILA) and indolepropionic acid (IPA), while inhibiting the production of indole. 2. **Carbohydrate Availability**: Simple carbohydrates, such as those found in pectin, inhibit indole production by repressing the expression of the tnaA gene in *Escherichia coli*. This inhibition allows more tryptophan to be available for other microorganisms, leading to increased production of ILA and IPA. 3. **Fiber Degradation**: *Bacteroides thetaiotaomicron* degrades pectin into monosaccharides, which cross-feed to *E. coli* and inhibit indole production through catabolite repression. This results in increased tryptophan availability for *Clostridium sporogenes*, which produces ILA and IPA. 4. **Human Studies**: In vivo experiments in gnotobiotic mice and human fecal cultures confirmed that dietary fiber reduces indole production while increasing ILA and IPA. This effect is consistent across different microbial communities and dietary fiber types. 5. **Mechanistic Model**: The study proposes a model explaining how dietary fiber interventions can shift gut microbial tryptophan metabolism towards beneficial metabolites. This model emphasizes the role of microbial competition, catabolite repression, and substrate availability in determining the balance between beneficial and potentially adverse metabolites. Overall, the findings provide a rationale for using dietary fiber interventions to promote the production of beneficial tryptophan metabolites and reduce the production of potentially harmful metabolites.