Division of Molecular/Experimental Radiology, Department of Radiology, Rheinische Friedrich-Wilhelms-University of Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, Germany.
EPMA J. 2010 Mar;1(1):130-7. doi: 10.1007/s13167-010-0015-4. Epub 2010 Mar 11.
Diabetes mellitus (DM) is a lifelong progressive disease with high morbidity and mortality worldwide. Whereas cardiovascular complications are well-known for DM, increasing evidence indicates that diabetics are predisposed to cancer. Understanding of molecular pathomechanisms of cancer in DM is of great importance. Dysregulation of glucose/insulin homeostasis leads to increased production of Reactive Oxygen/Nitrogen Species (ROS/RNS) and consequent damage to chromosomal/mitochondrial DNA, a frequent finding in DM. Long-term accumulation of modified/damaged DNA is well-acknowledged as triggering cancer. DNA-repair is a highly energy consuming process provoking increased mitochondrial activity. Particularly dangerous is a provoked activity of damaged mitochondria leading to a "vicious circle" lowering energy supply and potentiating ROS/RNS production. Mitochondrial dysfunction may be implicated in pathomechanisms of diabetes-related cancer. High risk for infectious disorders and induced viral proto-oncogenic activity may further contribute to cancer provocation. Much attention should be focused on preventive measures in diabetic healthcare, in order to restrict severe diabetes-related complications.
糖尿病（DM）是一种终身进行性疾病，在全球范围内具有较高的发病率和死亡率。虽然心血管并发症是 DM 的已知特征，但越来越多的证据表明糖尿病患者易患癌症。了解 DM 中癌症的分子发病机制非常重要。葡萄糖/胰岛素稳态失调会导致活性氧/氮物种（ROS/RNS）的产生增加，从而导致染色体/线粒体 DNA 损伤，这在 DM 中是常见的发现。长期积累修饰/受损的 DNA 已被广泛认为是引发癌症的原因。DNA 修复是一个高度耗能的过程，会引起线粒体活性增加。特别危险的是受损线粒体的活动引发“恶性循环”，降低能量供应并增强 ROS/RNS 的产生。线粒体功能障碍可能与糖尿病相关癌症的发病机制有关。感染性疾病的高风险和诱导的病毒原癌活性可能进一步促进癌症的发生。在糖尿病保健中，应高度重视预防措施，以限制严重的糖尿病相关并发症。
