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肥胖、糖尿病与癌症恶化。

Obesity, Diabetes, and Increased Cancer Progression.

机构信息

Touchstone Diabetes Center, Department of Internal Medicine, Dallas, TX, USA.

Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.

出版信息

Diabetes Metab J. 2021 Nov;45(6):799-812. doi: 10.4093/dmj.2021.0077. Epub 2021 Nov 22.

Abstract

Rates of obesity and diabetes have increased significantly over the past decades and the prevalence is expected to continue to rise further in the coming years. Many observations suggest that obesity and diabetes are associated with an increased risk of developing several types of cancers, including liver, pancreatic, endometrial, colorectal, and post-menopausal breast cancer. The path towards developing obesity and diabetes is affected by multiple factors, including adipokines, inflammatory cytokines, growth hormones, insulin resistance, and hyperlipidemia. The metabolic abnormalities associated with changes in the levels of these factors in obesity and diabetes have the potential to significantly contribute to the development and progression of cancer through the regulation of distinct signaling pathways. Here, we highlight the cellular and molecular pathways that constitute the links between obesity, diabetes, cancer risk and mortality. This includes a description of the existing evidence supporting the obesity-driven morphological and functional alternations of cancer cells and adipocytes through complex interactions within the tumor microenvironment.

摘要

在过去几十年中,肥胖症和糖尿病的发病率显著上升,预计未来几年这一患病率还将进一步上升。许多观察结果表明,肥胖症和糖尿病与多种癌症(包括肝癌、胰腺癌、子宫内膜癌、结直肠癌和绝经后乳腺癌)的发病风险增加有关。导致肥胖症和糖尿病的途径受到多种因素的影响,包括脂肪细胞因子、炎性细胞因子、生长激素、胰岛素抵抗和高血脂。与这些因素在肥胖症和糖尿病中的水平变化相关的代谢异常,通过调节不同的信号通路,有可能显著促进癌症的发生和发展。在这里,我们重点介绍构成肥胖、糖尿病、癌症风险和死亡率之间联系的细胞和分子途径。这包括描述现有证据,这些证据支持通过肿瘤微环境中的复杂相互作用,肥胖驱动癌细胞和脂肪细胞的形态和功能改变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/470b/8640143/bfad7158f538/dmj-2021-0077f1.jpg

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