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蔗糖对肝癌发病机制的有趣的肝保护作用。

Intriguing hepatoprotective effects of sucrose on hepatocellular carcinoma pathogenesis.

机构信息

Laboratorio de Enfermedades Hepáticas, Instituto Nacional de Medicina Genómica, Periférico Sur No. 4809, Col. Arenal Tepepan, Alcaldía Tlalpan, 14610, Ciudad de México, Mexico.

Departamento de Farmacología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Av. Instituto Politécnico Nacional 2508, 07360, Ciudad de México, Mexico.

出版信息

Sci Rep. 2024 Oct 10;14(1):23689. doi: 10.1038/s41598-024-74991-4.

DOI:10.1038/s41598-024-74991-4
PMID:39390131
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11467258/
Abstract

Chronic liver disease is closely linked to dietary intake factors, such as high consumption of simple carbohydrates including sucrose. In this study, the influence of sucrose on the development of hepatocellular carcinoma (HCC), the most common primary liver malignancy, was explored. Using the hepatocarcinogen diethylnitrosamine (DEN) to induce HCC in the rat, we co-administered sucrose with DEN. The co-administration significantly modified body, liver and pancreas weight, as well as, serum fatty acids and triglycerides. DEN caused liver structural alteration, fibrosis, and tumor formation; surprisingly, co-administration with sucrose restored hepatic lipids, improved liver architecture, and reduced fibrosis and tumor development. Sucrose intake negatively regulated tumor markers and cell proliferation, and reduced the expression of genes associated with lipid metabolism and oxidative stress response. These findings highlight a hepatoprotective effect of sucrose during DEN-induced hepatocarcinogenesis, underlining an intriguing role of high sucrose consumption during HCC development and providing new insights as well as possible pathways of cellular protection under sucrose intake on hepatocarcinogenesis.

摘要

慢性肝病与饮食摄入因素密切相关,例如大量摄入简单碳水化合物,包括蔗糖。本研究旨在探讨蔗糖对肝细胞癌(HCC)发展的影响,HCC 是最常见的原发性肝恶性肿瘤。我们使用肝癌致癌物二乙基亚硝胺(DEN)诱导大鼠 HCC,同时给予蔗糖和 DEN。联合给药显著改变了体重、肝脏和胰腺重量以及血清脂肪酸和甘油三酯。DEN 导致肝脏结构改变、纤维化和肿瘤形成;令人惊讶的是,与蔗糖联合给药可恢复肝脏脂质,改善肝脏结构,并减少纤维化和肿瘤发展。蔗糖摄入可负调控肿瘤标志物和细胞增殖,并降低与脂质代谢和氧化应激反应相关的基因表达。这些发现强调了蔗糖在 DEN 诱导的肝癌发生过程中的肝保护作用,提示在 HCC 发展过程中高蔗糖摄入具有引人注目的作用,并为蔗糖摄入在肝癌发生过程中对细胞的保护作用提供了新的见解和可能的途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/c22dcd297f0a/41598_2024_74991_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/8a054d5fe2b6/41598_2024_74991_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/84238af3f557/41598_2024_74991_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/9d010fbd1a36/41598_2024_74991_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/fb73f37b0676/41598_2024_74991_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/f78599f2e934/41598_2024_74991_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/b59230690751/41598_2024_74991_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/c22dcd297f0a/41598_2024_74991_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/8a054d5fe2b6/41598_2024_74991_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/84238af3f557/41598_2024_74991_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/9d010fbd1a36/41598_2024_74991_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/fb73f37b0676/41598_2024_74991_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/f78599f2e934/41598_2024_74991_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/b59230690751/41598_2024_74991_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fce0/11467258/c22dcd297f0a/41598_2024_74991_Fig7_HTML.jpg

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