ArticleToxins2026
Upstream Ecological Control of the IAA-Skatole Branch: A pH-Dependent Triple-Lock Framework for Gut-Derived Uremic Toxin Precursors.
Article in Toxins, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gut-derived indole metabolites are implicated in the gut-kidney axis, but the factors controlling the intestinal conversion of indole-3-acetic acid (IAA) to skatole remain incompletely defined. We developed a deterministic, hypothesis-generating framework that represents this conversion as a finite-pool allocation process governed by pH-dependent ecological permissiveness, terminal-conversion capacity, precursor availability, spatial progression, and competing loss. The model separates the available-pool scale from a dimensionless integrated conversion exposure, Ψ. Across 5400 loss-free scenarios spanning 10 pH profiles and graded metabolic and host-associated constraints, the distal endpoint normalized to the available pool followed the analytically derived relationship 1-exp-Ψ. Thus, distinct combinations of mechanistically relevant parameters produced the same normalized distal endpoint, demonstrating that this endpoint alone cannot uniquely identify the underlying mechanism. Competing loss further separated absolute, total-pool-normalized, and conditional outputs, showing that mechanistic interpretation depends on endpoint normalization. Analytical and numerical checks supported internal consistency. The framework was not fitted to biological data, and concentration values were used only as technical scaling references. This biologically unvalidated model generates experimentally testable hypotheses regarding the roles of pH, terminal-conversion capacity, precursor availability, and competing loss in intestinal IAA-to-skatole metabolism; it is not intended to provide physiological or clinical predictions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.