Noto Hiroshi, Raskin Philip
Division of Endocrinology and Metabolism, Department of Internal Medicine, The University of Texas Southwestern Medical Center at Dallas, TX 75390-8858, USA.
J Diabetes Complications. 2006 Mar-Apr;20(2):113-20. doi: 10.1016/j.jdiacomp.2006.01.001.
Since the discovery of the hepatitis C virus (HCV) in 1989, attention has been paid to the association of chronic HCV infection and the development of diabetes. The risk factors for diabetes include older age, HCV genotype 3, severe liver fibrosis, family history of diabetes, and liver/kidney transplantation. Emerging evidence in animals and humans has shown that HCV infection induces hepatic steatosis and increases tumor necrosis factor-alpha level, both resulting in the development of insulin resistance and subsequent type 2 diabetes. It is suggested that the presence of diabetes and hepatic steatosis may enhance fibrosis progression, hepatocellular carcinoma, and atherosclerosis. Interferon is reportedly associated with improved glucose tolerance. However, interferon might enhance underlying autoimmunity against beta cells, leading to overt type 1 diabetes that is genetically predisposed or give rise to hyperglycemia, resulting in the development of type 2 diabetes. In light of the national epidemic of type 2 diabetes, the link between HCV and diabetes would be a major public health problem. Further clinical researches are awaited in order to effectively detect, prevent, and treat HCV-associated type 2 diabetes, which would also slow the progression of hepatitis C itself.
自1989年丙型肝炎病毒（HCV）被发现以来，慢性HCV感染与糖尿病发生之间的关联就受到了关注。糖尿病的危险因素包括高龄、HCV 3型、严重肝纤维化、糖尿病家族史以及肝/肾移植。动物和人类的新证据表明，HCV感染会诱发肝脂肪变性并提高肿瘤坏死因子-α水平，二者均会导致胰岛素抵抗的发生以及随后的2型糖尿病。有研究提示，糖尿病和肝脂肪变性的存在可能会加速肝纤维化进展、肝细胞癌发生以及动脉粥样硬化。据报道，干扰素与糖耐量改善有关。然而，干扰素可能会增强针对β细胞的潜在自身免疫反应，导致具有遗传易感性的显性1型糖尿病，或引发高血糖，进而导致2型糖尿病的发生。鉴于2型糖尿病在全国的流行情况，HCV与糖尿病之间的联系将成为一个重大的公共卫生问题。有待进一步开展临床研究，以便有效地检测、预防和治疗HCV相关的2型糖尿病，这也将减缓丙型肝炎本身的进展。
