ArticlePloS one2014
Diabetes promotes DMH-induced colorectal cancer by increasing the activity of glycolytic enzymes in rats.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Silymarin and Zinc Oxide Nanoparticles Attenuate Experimental Colon Cancer in Rats Through Crosstalk of miR-192 and β-Catenin Pathways.Biomolecules · 2026Article
- Poorly controlled type II diabetes mellitus significantly enhances postoperative chemoresistance in patients with stage III colon cancer.World journal of gastroenterology · 2025Article
- Gene coexpression network analysis identified potential biomarkers in gestational diabetes mellitus progression.Molecular genetics & genomic medicine · 2019Article
- Oxidative stress induced autophagy in cancer associated fibroblast enhances proliferation and metabolism of colorectal cancer cells.Cell cycle (Georgetown, Tex.) · 2017Article
- Metformin prevents DMH-induced colorectal cancer in diabetic rats by reversing the warburg effect.Cancer medicine · 2015Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objective of the present study was to investigate the association between diabetes mellitus and colorectal carcinogenesis as well as the possible mechanism involved in this interaction. Diabetes rat models were induced with a low dose of STZ followed by a low dose of DMH to induce colorectal cancer. The formation of ACF in the colon and the incidence, number and size of tumors were measured. The activity of glycolytic enzymes in colonic tissues was also measured. The results demonstrated that both the total number of ACF and the number of foci that contain a different number of crypts were increased in diabetic rats. At the end of the experimental treatment, the incidence, number and size of tumors were also increased in diabetic rats. Overall, these data indicated that diabetes increased the risk of colorectal cancer. The activity of HK and PK in colonic tissues was increased in diabetic rats, whereas the activity of PDH was decreased. In addition, the activities of these enzymes in intratumor were higher than that of in peritumor. These data indicated that the high rate of glycolysis may play a role in colorectal carcinogenesis in diabetic rats.
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