ArticleJournal of gastroenterology2024
Resistant starch reduces glycolysis by HK2 and suppresses high-fructose corn syrup-induced colon tumorigenesis.
Article in Journal of gastroenterology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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.
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Who cites it
6 citing papers in PubMed.
- Dietary Fructose and Early-Onset Colorectal Cancer: Metabolic, Microbial, and Translational Perspectives.Microorganisms · 2026Review
- [HeZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025Article
- Anticancer potential of dietary fiber for colorectal carcinoma: a narrative review.Annals of medicine · 2025Review
- Comparison of the Structure, Physicochemical Properties, and Impact on Intestinal Flora of Processed and UnprocessedFoods (Basel, Switzerland) · 2025Article
- Fructose Metabolism in Cancer: Molecular Mechanisms and Therapeutic Implications.International journal of medical sciences · 2025Review
- Microbiota-host metabolism reprogramming in colorectal cancer: from pathogenesis to precision therapies.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundThe intake of high-fructose corn syrup (HFCS) may increase the risk of colorectal cancer (CRC). This study aimed to explore the potential effects and mechanisms of resistant starch (RS) in HFCS-induced colon tumorigenesis.
methodsThe azoxymethane/dextran sodium sulfate (AOM/DSS) and Apc
resultsRS suppressed HFCS-induced colon tumorigenesis through reshaping the microbial community. Mechanistically, the alteration of the microbial community after RS supplement increased the levels of intestinal SCFAs, especially butyrate, leading to the suppression of glycolysis and CRC cell proliferation by downregulating HK2.
conclusionsOur study identified RS as a candidate of protective factors in CRC and may provide a potential target for HFCS-related CRC treatment.
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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.