Insulin resistance and cancer risk: an overview of the pathogenetic mechanisms.
Insulin resistance and cancer risk: an overview of the pathogenetic mechanisms.
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DOI：
10.1155/2012/789174
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发表时间：
2012
影响因子：
--
通讯作者：
Brunetti A
中科院分区：
文献类型：
--
作者：
Arcidiacono B;Iiritano S;Nocera A;Possidente K;Nevolo MT;Ventura V;Foti D;Chiefari E;Brunetti A
胰岛素抵抗在肥胖或 2 型糖尿病 (T2D) 患者中很常见，这些患者的循环胰岛素水平经常升高。最近的流行病学和临床证据表明胰岛素抵抗与癌症之间存在联系。这种关联的机制尚不清楚，但高胰岛素血症（胰岛素抵抗的标志）和生物可利用的胰岛素样生长因子 I (IGF-I) 的增加似乎在胰岛素抵抗患者的肿瘤发生和进展中发挥作用。胰岛素和 IGF-I 抑制肝脏合成性激素结合球蛋白 (SHBG)，而这两种激素刺激卵巢合成性类固醇，其在乳腺上皮和子宫内膜中的作用可以促进细胞增殖并抑制细胞凋亡。此外，胰岛素抵抗患者患癌症的风险增加可能是由于活性氧 (ROS) 产生过多，活性氧会损害 DNA，从而导致突变和癌变。另一方面，肥胖和糖尿病患者的脂肪组织中大量的炎症细胞可能会促进全身炎症，从而导致促肿瘤环境。在这里，我们总结了胰岛素抵抗和癌症的最新进展，重点关注最近描述的各种相关机制，并讨论这些机制如何促进癌症的发生和进展。
Insulin resistance is common in individuals with obesity or type 2 diabetes (T2D), in which circulating insulin levels are frequently increased. Recent epidemiological and clinical evidence points to a link between insulin resistance and cancer. The mechanisms for this association are unknown, but hyperinsulinaemia (a hallmark of insulin resistance) and the increase in bioavailable insulin-like growth factor I (IGF-I) appear to have a role in tumor initiation and progression in insulin-resistant patients. Insulin and IGF-I inhibit the hepatic synthesis of sex-hormone binding globulin (SHBG), whereas both hormones stimulate the ovarian synthesis of sex steroids, whose effects, in breast epithelium and endometrium, can promote cellular proliferation and inhibit apoptosis. Furthermore, an increased risk of cancer among insulin-resistant patients can be due to overproduction of reactive oxygen species (ROS) that can damage DNA contributing to mutagenesis and carcinogenesis. On the other hand, it is possible that the abundance of inflammatory cells in adipose tissue of obese and diabetic patients may promote systemic inflammation which can result in a protumorigenic environment. Here, we summarize recent progress on insulin resistance and cancer, focusing on various implicated mechanisms that have been described recently, and discuss how these mechanisms may contribute to cancer initiation and progression.
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