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抗性淀粉通过 HK2 抑制糖酵解，从而抑制高果糖玉米糖浆诱导的结肠肿瘤发生。

Resistant starch reduces glycolysis by HK2 and suppresses high-fructose corn syrup-induced colon tumorigenesis.

机构信息

Department of Gastroenterology, Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China.

Department of Pathology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.

出版信息

J Gastroenterol. 2024 Oct;59(10):905-920. doi: 10.1007/s00535-024-02138-3. Epub 2024 Aug 14.

DOI:10.1007/s00535-024-02138-3
PMID:39141107
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11415400/
Abstract

BACKGROUND

The 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.

METHODS

The azoxymethane/dextran sodium sulfate (AOM/DSS) and Apc mice models were used to investigate the roles of HFCS and RS in CRC in vivo. An immunohistochemistry (IHC) staining analysis was used to detect the expression of proliferation-related proteins in tissues. 16S rRNA sequencing for microbial community, gas chromatography for short-chain fatty acids (SCFAs), and mass spectrometry analysis for glycolysis products in the intestines were performed. Furthermore, lactic acid assay kit was used to detect the glycolysis levels in vitro.

RESULTS

RS 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.

CONCLUSIONS

Our study identified RS as a candidate of protective factors in CRC and may provide a potential target for HFCS-related CRC treatment.

摘要

背景

摄入高果糖玉米糖浆（HFCS）可能会增加结直肠癌（CRC）的风险。本研究旨在探讨抗性淀粉（RS）在 HFCS 诱导的结肠癌发生中的潜在作用和机制。

方法

使用氧化偶氮甲烷/葡聚糖硫酸钠（AOM/DSS）和 Apc 小鼠模型在体内研究 HFCS 和 RS 在 CRC 中的作用。免疫组织化学（IHC）染色分析用于检测组织中与增殖相关的蛋白表达。对微生物群落进行 16S rRNA 测序，对短链脂肪酸（SCFAs）进行气相色谱分析，对肠道中的糖酵解产物进行质谱分析。此外，使用乳酸测定试剂盒检测体外糖酵解水平。

结果

RS 通过重塑微生物群落抑制 HFCS 诱导的结肠癌发生。在机制上，RS 补充后微生物群落的改变增加了肠道 SCFAs 的水平，特别是丁酸盐，通过下调 HK2 抑制糖酵解和 CRC 细胞增殖。

结论

本研究确定 RS 是 CRC 中保护性因素的候选物，可能为 HFCS 相关 CRC 治疗提供潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb53/11415400/9df159e2e19d/535_2024_2138_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb53/11415400/47a4f1ea7d98/535_2024_2138_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb53/11415400/006968b60ce9/535_2024_2138_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb53/11415400/101a2ece8873/535_2024_2138_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb53/11415400/810760199dbd/535_2024_2138_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb53/11415400/9df159e2e19d/535_2024_2138_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb53/11415400/47a4f1ea7d98/535_2024_2138_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb53/11415400/aff8d8547e8a/535_2024_2138_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb53/11415400/006968b60ce9/535_2024_2138_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb53/11415400/101a2ece8873/535_2024_2138_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb53/11415400/810760199dbd/535_2024_2138_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb53/11415400/9df159e2e19d/535_2024_2138_Fig6_HTML.jpg

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