Wainwright P, Scorletti E, Byrne C D
Clinical Biochemistry, University Hospital Southampton, Southampton, UK.
Chemical Pathology and Metabolic Medicine, Department of Laboratory Medicine, D-Level Pathology Block, University Hospital Southampton, Tremona Road, Southampton, SO16 6YD, UK.
Curr Diab Rep. 2017 Apr;17(4):20. doi: 10.1007/s11892-017-0851-x.
This review aims to assess the epidemiological evidence for a link between type 2 diabetes and hepatocellular carcinoma and to investigate possible pathophysiological mechanisms.
The presence of type 2 diabetes significantly increases the risk of developing hepatocellular carcinoma, and treatment with metformin may be associated with a lower risk. Treatment with insulin and sulphonylureas may be associated with increased risk. The pathophysiology underlying development of hepatocellular carcinoma in this context is complex and is likely to involve increased proinflammatory mediators, oxidative stress, JNK-1 activation, increased IGF-1 activity, altered gut microbiota and immunomodulation. Hepatocellular carcinoma incidence is increasing and this is likely to be linked to the increasing incidence of type 2 diabetes, obesity and the metabolic syndrome. These conditions increase the risk of developing hepatocellular carcinoma, and a greater understanding of the underlying pathophysiology may help with the development of novel treatments.
本综述旨在评估2型糖尿病与肝细胞癌之间联系的流行病学证据，并探究可能的病理生理机制。
2型糖尿病的存在显著增加了发生肝细胞癌的风险，二甲双胍治疗可能与较低风险相关。胰岛素和磺脲类药物治疗可能与风险增加相关。在这种情况下，肝细胞癌发生的病理生理学很复杂，可能涉及促炎介质增加、氧化应激、JNK-1激活、IGF-1活性增加、肠道微生物群改变和免疫调节。肝细胞癌发病率正在上升，这可能与2型糖尿病、肥胖症和代谢综合征发病率的增加有关。这些情况增加了发生肝细胞癌的风险，对潜在病理生理学的更深入了解可能有助于开发新的治疗方法。
