代谢综合征与结直肠息肉相关性的研究进展
Research Progress on the Correlation between Metabolic Syndrome and Colorectal Polyps
DOI: 10.12677/acm.2024.143901, PDF,   
作者: 王欣然, 桑荣霞:石家庄市人民医院消化内科,河北 石家庄
关键词: 代谢综合征结直肠息肉Metabolic Syndrome Colorectal Polyps
摘要: 代谢综合征(MetS)是包括肥胖、糖尿病、高血压、血脂异常等多种代谢疾病在内的一组临床综合征。结直肠息肉是结直肠粘膜突出肠腔的隆起性病变,依据病理特征可将其分为腺瘤性息肉和非腺瘤性息肉。现有研究表明,腺瘤性息肉进一步发展可致结直肠癌(CRC)。MetS被认为是CRC发生和发展的危险因素。近年来,有关研究针对MetS与结直肠息肉的关系展开,本文综述了MetS与结直肠息肉的相关性,同时对研究前景进行展望。
Abstract: Metabolic syndrome (MetS) is a group of clinical syndromes including obesity, diabetes, hypertension, dyslipidemia and other metabolic diseases. Colorectal polyps are raised lesions of the colorectal mucosa protruding from the intestinal lumen and can be divided into adenomatous polyps and non-adenomatous polyps according to pathological features. Existing studies have shown that further development of adenomatous polyps can lead to colorectal cancer (CRC). MetS is considered a risk factor for the occurrence and progression of CRC. In recent years, relevant studies have focused on the relationship between MetS and colorectal polyps, and this article reviews the correlation between MetS and colorectal polyps, and looks forward to the research prospects.
文章引用:王欣然, 桑荣霞. 代谢综合征与结直肠息肉相关性的研究进展[J]. 临床医学进展, 2024, 14(3): 1733-1740. https://doi.org/10.12677/acm.2024.143901

参考文献

[1] 李晓景, 高孝忠, 褚衍六, 等. 结直肠癌合并高风险性腺瘤内镜治疗时机的临床研究[J]. 中华胃肠内镜电子杂志, 2021, 8(1): 13-17.
[2] Nakamura, F., Sato, Y., Okamoto, K., et al. (2022) Colorectal Carcinoma Occurring via the Adenoma-Carcinoma Pathway in Patients with Serrated Polyposis Syndrome. Journal of Gastroenterology, 57, 286-299. [Google Scholar] [CrossRef] [PubMed]
[3] Baidoun, F., Elshiwy, K., Elkeraie, Y., et al. (2021) Colorectal Cancer Epidemiology: Recent Trends and Impact on Outcomes. Current Drug Targets, 22, 998-1009. [Google Scholar] [CrossRef
[4] 吴艳惠, 杨鑫, 吴现瑞. 代谢综合征与结直肠癌相关性的研究进展[J]. 中国肿瘤外科杂志, 2023, 15(3): 262-265.
[5] Breau, G. and Ellis, U. (2020) Risk Factors Associated with Young-Onset Colorectal Adenomas and Cancer: A Systematic Review and Meta-Analysis of Observational Research. Cancer Control, 27. [Google Scholar] [CrossRef] [PubMed]
[6] Fliss-Isakov, N., Zelber-Sagi, S., Webb, M., et al. (2017) Distinct Metabolic Profiles Are Associated with Colorectal Adenomas and Serrated Polyps. Obesity, 25, S72-S80. [Google Scholar] [CrossRef] [PubMed]
[7] Hirode, G. and Wong, R, J. (2020) Trends in the Prevalence of Metabolic Syndrome in the United States, 2011-2016. JAMA, 323, 2526-2528. [Google Scholar] [CrossRef] [PubMed]
[8] 钏莉雪, 常江, 赵锦涵. 代谢综合征与结直肠腺瘤性息肉的相关性研究[J]. 胃肠病学, 2019, 24(11): 699-702.
[9] Ozkan, N.T., Tokmak, A., Guzel, A.I., et al. (2015) The Association between Endometrial Polyps and Metabolic Syndrome: A Case-Control Study. Australian and New Zealand Journal of Obstetrics and Gynaecology, 55, 274-278. [Google Scholar] [CrossRef] [PubMed]
[10] Bueloni-Dias, F.N., Spadoto-Dias, D., Delmanto, L.R., et al. (2016) Metabolic Syndrome as a Predictor of Endometrial Polyps in Postmenopausal Women. Menopause, 23, 759-764. [Google Scholar] [CrossRef
[11] Chen, Y., Wang, T., Gao, R., et al. (2023) Effects of Metabolic Syndrome and Its Components on the Postoperative Recurrence in Chronic Rhinosinusitis with Nasal Polyps’ Patients. Brazilian Journal of Otorhinolaryngology, 90, Article ID: 101371. [Google Scholar] [CrossRef] [PubMed]
[12] Jia, W.P., Xiang, K.S., Chen, L., et al. (2002) Epidemiological Study on Obesity and Its Comorbidities in Urban Chinese Older Than 20 Years of Age in Shanghai, China. Obesity Reviews, 3, 157-165. [Google Scholar] [CrossRef
[13] Moon, J.M., Im, J.P., Kim, D., et al. (2021) Increasing Changes in Visceral Adiposity Is Associated with Higher Risk for Colorectal Adenoma: Multilevel Analysis in a Prospective Cohort. Journal of Gastroenterology and Hepatology, 36, 1836-1842. [Google Scholar] [CrossRef] [PubMed]
[14] Jung, I.S., Shin, C.M., Park, S.J., et al. (2019) Association of Visceral Adiposity and Insulin Resistance with Colorectal Adenoma and Colorectal Cancer. Intestinal Research, 17, 404-412. [Google Scholar] [CrossRef] [PubMed]
[15] 吴文琪, 万远太. 结直肠息肉发生发展相关因素的研究现状[J]. 消化肿瘤杂志(电子版), 2021, 13(2): 148-152.
[16] Kasprzak, A. (2021) Insulin-Like Growth Factor 1 (IGF-1) Signaling in Glucose Metabolism in Colorectal Cancer. International Journal of Molecular Sciences, 22, Article 6434. [Google Scholar] [CrossRef] [PubMed]
[17] Alagaratnam, S., Loizidou, M., Yang, S.Y., et al. (2020) Increased Expression of IGF-1Ec with Increasing Colonic Polyp Dysplasia and Colorectal Cancer. Journal of Cancer Research and Clinical Oncology, 146, 2861-2870. [Google Scholar] [CrossRef] [PubMed]
[18] Qin, M., Wang, H.P., Song, B., et al. (2021) [Relationship between Insulin Resistance, Serum VCAM-1, FGF19, IGF-1 and Colorectal Polyps]. Chinese Journal of Oncology, 43, 553-562.
[19] Brown, J.C. (1982) Gastric Inhibitory Polypeptide. Springer, Berlin. [Google Scholar] [CrossRef
[20] Dupre, J., Ross, S, A., Watson, D., et al. (1973) Stimulation of Insulin Secretion by Gastric Inhibitory Polypeptide in Man. The Journal of Clinical Endocrinology & Metabolism, 37, 826-828. [Google Scholar] [CrossRef] [PubMed]
[21] Sasaki, Y., Takeda, H., Sato, T., et al. (2011) Increased Levels of Serum Glucose-Dependent Insulinotropic Polypeptide as a Novel Risk Factor for Human Colorectal Adenoma. Metabolism, 60, 1253-1258. [Google Scholar] [CrossRef] [PubMed]
[22] Rogers, M., Gill, D., Ahlqvist, E., et al. (2023) Genetically Proxied Impaired GIPR Signaling and Risk of 6 Cancers. iScience, 26, Article ID: 106848. [Google Scholar] [CrossRef] [PubMed]
[23] Chen, F.P., Wang, H.M., Chiang, F.F., et al. (2014) The Metabolic Syndrome Is Associated with an Increased Risk of Colorectal Polyps Independent of Plasma Homocysteine. Annals of Nutrition and Metabolism, 64, 106-112. [Google Scholar] [CrossRef] [PubMed]
[24] Zhang, R., Yin, J., Huo, C., et al. (2022) The Relationship between Colorectal Polyps and Serum Lipid Levels: A Systematic Review and Meta-Analysis. Journal of Clinical Gastroenterology, 56, 654-667. [Google Scholar] [CrossRef
[25] Tang, C.T., Li, J., Yang, Z., et al. (2022) Comparison of Some Biochemical Markers between Early-Onset and Late-Onset Colorectal Precancerous Lesions: A Single-Center Retrospective Study. Journal of Clinical Laboratory Analysis, 36, e24637. [Google Scholar] [CrossRef] [PubMed]
[26] Crespo-Sanjuan, J., Calvo-Nieves, M.D., Aguirre-Gervas, B., et al. (2015) Early Detection of High Oxidative Activity in Patients with Adenomatous Intestinal Polyps and Colorectal Adenocarcinoma: Myeloperoxidase and Oxidized Low-Density Lipoprotein in Serum as New Markers of Oxidative Stress in Colorectal Cancer. Laboratory Medicine, 46, 123-135. [Google Scholar] [CrossRef
[27] Chen, H., Zhou, H., Liang, Y., et al. (2023) UHPLC-HRMS-Based Serum Untargeted Lipidomics: Phosphatidylcholines and Sphingomyelins Are the Main Disturbed Lipid Markers to Distinguish Colorectal Advanced Adenoma from Cancer. Journal of Pharmaceutical and Biomedical Analysis, 234, Article ID: 115582. [Google Scholar] [CrossRef] [PubMed]
[28] Zhu, Y., Wang, L., Nong, Y., et al. (2021) Serum Untargeted UHPLC-HRMS-Based Lipidomics to Discover the Potential Biomarker of Colorectal Advanced Adenoma. Cancer Management and Research, 13, 8865-8878. [Google Scholar] [CrossRef
[29] Chen, H.Y., Lee, W.H., Hsu, H.L., et al. (2022) Arterial Stiffness Is Associated with High-Risk Colorectal Adenomas and Serrated Lesions: A Cross-Sectional Study in a Taiwanese Population. Journal of Cardiology, 80, 139-144. [Google Scholar] [CrossRef] [PubMed]
[30] Yamaji, Y., Mitsushima, T. and Koike, K. (2014) Pulse-Wave Velocity, the Ankle-Brachial Index, and the Visceral Fat Area Are Highly Associated with Colorectal Adenoma. Digestive and Liver Disease, 46, 943-949. [Google Scholar] [CrossRef] [PubMed]
[31] Boden, G., Homko, C., Barrero, C.A., et al. (2015) Excessive Caloric Intake Acutely Causes Oxidative Stress, GLUT4 Carbonylation, and Insulin Resistance in Healthy Men. Science Translational Medicine, 7, 304re7. [Google Scholar] [CrossRef] [PubMed]
[32] Xu, H., Li, X., Adams, H., et al. (2018) Etiology of Metabolic Syndrome and Dietary Intervention. International Journal of Molecular Sciences, 20, Article 128. [Google Scholar] [CrossRef] [PubMed]
[33] Boldogh, I., Hajas, G., Aguilera-Aguirre, L., et al. (2012) Activation of Ras Signaling Pathway by 8-Oxoguanine DNA Glycosylase Bound to Its Excision Product, 8-Oxoguanine. Journal of Biological Chemistry, 287, 20769-20773. [Google Scholar] [CrossRef
[34] German, P., Szaniszlo, P., Hajas, G., et al. (2013) Activation of Cellular Signaling by 8-Oxoguanine DNA Glycosylase-1-Initiated DNA Base Excision Repair. DNA Repair, 12, 856-863. [Google Scholar] [CrossRef] [PubMed]
[35] Wang, T., Brown, N.M., McCoy, A.N., et al. (2022) ω-3 Polyunsaturated Fatty Acids, Gut Microbiota, Microbial Metabolites, and Risk of Colorectal Adenomas. Cancers, 14, Article 4443. [Google Scholar] [CrossRef] [PubMed]
[36] Finucane, O.M., Lyons, C.L., Murphy, A.M., et al. (2015) Monounsaturated Fatty Acid-Enriched High-Fat Diets Impede Adipose NLRP3 Inflammasome-Mediated IL-1β Secretion and Insulin Resistance Despite Obesity. Diabetes, 64, 2116-2128. [Google Scholar] [CrossRef] [PubMed]
[37] Wang, J., Tang, H., Zhang, C., et al. (2015) Modulation of Gut Microbiota during Probiotic-Mediated Attenuation of Metabolic Syndrome in High Fat Diet-Fed Mice. The ISME Journal, 9, 1-15. [Google Scholar] [CrossRef] [PubMed]
[38] Hulston, C.J., Churnside, A.A. and Venables, M.C. (2015) Probiotic Supplementation Prevents High-Fat, Overfeeding-Induced Insulin Resistance in Human Subjects. British Journal of Nutrition, 113, 596-602. [Google Scholar] [CrossRef
[39] Chassaing, B., Miles-Brown, J., Pellizzon, M., et al. (2015) Lack of Soluble Fiber Drives Diet-Induced Adiposity in Mice. American Journal of Physiology-Gastrointestinal and Liver Physiology, 309, G528-G541. [Google Scholar] [CrossRef] [PubMed]
[40] Yan, H., Potu, R., Lu, H., et al. (2013) Dietary Fat Content and Fiber Type Modulate Hind Gut Microbial Community and Metabolic Markers in the Pig. PLOS ONE, 8, e59581. [Google Scholar] [CrossRef] [PubMed]
[41] Gutting, T., Weber, C.A., Weidner, P., et al. (2018) PPARgamma-Activation Increases Intestinal M1 Macrophages and Mitigates Formation of Serrated Adenomas in Mutant KRAS Mice. Oncoimmunology, 7, e1423168. [Google Scholar] [CrossRef
[42] Kurnaz-Gomleksiz, O., Torun, B.C., Isbir, T., et al. (2022) The Role of PPAR-Gamma C161T Polymorphism in Colorectal Cancer Susceptibility. In Vivo, 36, 1911-1915. [Google Scholar] [CrossRef] [PubMed]
[43] Barry, E.L., Fedirko, V., Uppal, K., et al. (2020) Metabolomics Analysis of Aspirin’s Effects in Human Colon Tissue and Associations with Adenoma Risk. Cancer Prevention Research, 13, 863-876. [Google Scholar] [CrossRef
[44] Phua, L.C., Chue, X.P., Koh, P.K., et al. (2014) Non-Invasive Fecal Metabonomic Detection of Colorectal Cancer. Cancer Biology & Therapy, 15, 389-397. [Google Scholar] [CrossRef] [PubMed]
[45] Denkert, C., Budczies, J., Weichert, W., et al. (2008) Metabolite Profiling of Human Colon Carcinoma—Deregulation of TCA Cycle and Amino Acid Turnover. Molecular Cancer, 7, Article No. 72. [Google Scholar] [CrossRef] [PubMed]
[46] Hirayama, A., Kami, K., Sugimoto, M., et al. (2009) Quantitative Metabolome Profiling of Colon and Stomach Cancer Microenvironment by Capillary Electrophoresis Time-of-Flight Mass Spectrometry. Cancer Research, 69, 4918-4925. [Google Scholar] [CrossRef
[47] Weir, T.L., Manter, D.K., Sheflin, A.M., et al. (2013) Stool Microbiome and Metabolome Differences between Colorectal Cancer Patients and Healthy Adults. PLOS ONE, 8, e70803. [Google Scholar] [CrossRef] [PubMed]
[48] Wang, X., Wang, J., Rao, B. and Deng, L. (2022) Gut Flora Profiling and Fecal Metabolite Composition of Colorectal Cancer Patients and Healthy Individuals. Experimental and Therapeutic Medicine, 23, Article No. 250. [Google Scholar] [CrossRef] [PubMed]
[49] Yang, M., Liu, S. and Zhang, C. (2022) The Related Metabolic Diseases and Treatments of Obesity. Healthcare, 10, Article 1616. [Google Scholar] [CrossRef] [PubMed]