Department of Medicine, Division of Endocrinology, Mt Sinai School of Medicine, New York, New York 10029-6574, USA.
Curr Opin Endocrinol Diabetes Obes. 2013 Oct;20(5):485-94. doi: 10.1097/01.med.0000433065.16918.83.
The aim of this review article is to discuss the epidemiological links between diabetes and cancer; the potential biological mechanisms linking diabetes, obesity and cancer; the risk of cancer associated with antidiabetic medications.
The data discussed in this review were obtained from the American Association of Clinical Endocrinologists Consensus Conference on Diabetes and Cancer, held in New York, NY, USA, September 2012.
The results of these studies demonstrate a significant association between diabetes and the risk of multiple cancers, including hepatocellular, pancreatic, endometrial, colorectal, breast, kidney, bladder, gastric, and ovarian cancer, non-Hodgkin lymphoma, T cell lymphoma and leukemia. There are multiple potential biological mechanisms that may link type 2 diabetes, obesity and cancer. Insulin resistance and hyperinsulinemia may lead to direct activation of the insulin receptors on tumor cells and promote tumor growth. Other potential mechanisms include increased circulating, local or bioavailable insulin-like growth factor 1, hyperglycemia, dyslipidemia, increased circulating or local estrogen, adipokines and direct and indirect effects of inflammatory cytokines. Epidemiological studies have had conflicting results regarding the associations between various classes of antidiabetic medication and cancer development. Animal studies have demonstrated increased tumor growth with certain medications, but their relevance to humans is uncertain. Metformin may, however, have protective effects on cancer development and may improve survival in patients with cancer.
We describe the current understanding of the links among diabetes, antidiabetic medication and cancer risk. We highlight some of the issues that should be addressed in the future to prevent cancer development and death in those with diabetes.
本文旨在讨论糖尿病与癌症之间的流行病学联系；糖尿病、肥胖与癌症之间潜在的生物学机制；以及降糖药物与癌症风险之间的关联。
本文所讨论的数据来源于美国临床内分泌医师协会 2012 年 9 月在纽约举行的糖尿病与癌症共识会议。
这些研究的结果表明，糖尿病与多种癌症的风险显著相关，包括肝癌、胰腺癌、子宫内膜癌、结直肠癌、乳腺癌、肾癌、膀胱癌、胃癌和卵巢癌、非霍奇金淋巴瘤、T 细胞淋巴瘤和白血病。有多种潜在的生物学机制可能将 2 型糖尿病、肥胖和癌症联系起来。胰岛素抵抗和高胰岛素血症可能导致肿瘤细胞上胰岛素受体的直接激活，并促进肿瘤生长。其他潜在机制包括循环、局部或生物可利用的胰岛素样生长因子 1 增加、高血糖、血脂异常、循环或局部雌激素增加、脂肪细胞因子以及炎症细胞因子的直接和间接作用。关于各种类别的降糖药物与癌症发展之间的关联，流行病学研究结果存在矛盾。动物研究表明某些药物会增加肿瘤生长，但它们对人类的相关性尚不确定。然而，二甲双胍可能对癌症发展具有保护作用，并可能改善癌症患者的生存。
本文描述了目前对糖尿病、降糖药物与癌症风险之间关联的理解。我们强调了未来应该解决的一些问题，以预防糖尿病患者癌症的发生和死亡。
