ArticlePoultry science2026
Dietary supplementation with raw potato starch reversed enteritis-induced bone loss via Malt1 paracaspase inhibition in meat ducks.
Article in Poultry science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intestinal inflammation is a key driver of progressive bone deterioration, elevating the risk of fractures and chronic pain in meat ducks. As a fermentable type II resistant starch, raw potato starch (RPS) probably supports gut health and potentially mitigate this inflammatory bone loss. In this study, an enteritis model was established in meat ducks using dextran sodium sulphate (DSS) and to assess its effect on bone metabolism, as well as to determine the role of RPS in enteritis-mediated bone loss. In enteritis-induced meat duck models, dietary supplementation with 12% RPS reversed intestinal inflammation‑induced bone loss, an effect accompanied by improved intestinal homeostasis and reduced bone resorption (P < 0.05). These changes were associated with alterations in inflammatory cytokine secretion, osteoclastic differentiation, and the mucosa-associated lymphoid tissue 1 (Malt1) mediated nuclear factor kappa-B (NF-κB) pathway, as supported by transcriptional analysis of the bone marrow and AlphaFold predictions. To elucidate the mechanism by which RPS restores bone mass in the DSS-treated ducks, a specific Malt1 inhibitor (mepazine) was employed. Ducks were fed either a basal diet or a 12% RPS diet, with or without supplemental mepazine at 20 mg/kg body weight, and all were challenged with DSS from d 7 to 21. Herein, with unchanged expressions of regulatory T cell cytokines (P > 0.05), Malt1 protease inactivation or dietary RPS supplementation enhanced tibia ash and bone volume in metaphysis (Both P < 0.05). Along with increased Firmicutes levels and the production of short chain fatty acids (P < 0.05), mepazine or dietary RPS inclusion downregulated NF-κB inflammatory pathway, resulting in decreased the osteoclastic activity. Co-treatment with mepazine and RPS further amplified this effect, implicating Malt1 protease inhibition as the mechanism by which RPS protects against enteritis-induced osteopenia. These findings revealed that diet contained 12% RPS reverses enteritis-induced bone loss in meat ducks, likely by inhibiting Malt1 paracaspase and subsequently suppressing NF-κB pathway-mediated bone resorption.
Indexed as
Identifiers
What OpenQuestion holds
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.