Clark Jeanne M, Diehl Anna Mae
Department of Medicine, Johns Hopkins University School of Medicine, 912 Ross Building, 720 Rutland Street, Baltimore, MD 21205, USA.
Curr Diab Rep. 2002 Jun;2(3):210-5. doi: 10.1007/s11892-002-0085-3.
Type 2 diabetes is strongly associated with nonalcoholic fatty liver disease (NAFLD), a spectrum of liver damage that ranges from relatively benign hepatic steatosis to potentially fatal cirrhosis. The severities of insulin resistance and liver damage parallel each other, with the greatest prevalence of cirrhosis occurring in cirrhotics. However, it is unknown whether one of these conditions causes the other, or if both are consequences of another process. Experimental evidence suggests that both insulin resistance and NAFLD result from a chronic inflammatory state. The mechanisms driving this chronic inflammation are unknown but might include the egress of products from intestinal bacteria into the portal blood, liver, and systemic circulation to trigger a sustained inflammatory cytokine response in genetically susceptible individuals. More research is needed to evaluate this hypothesis and to determine the benefits of treatments that interrupt this pathogenic cascade.
2型糖尿病与非酒精性脂肪性肝病（NAFLD）密切相关，NAFLD是一种肝脏损伤范围，从相对良性的肝脂肪变性到潜在致命的肝硬化。胰岛素抵抗和肝脏损伤的严重程度相互平行，肝硬化在肝硬化患者中患病率最高。然而，尚不清楚这些情况之一是否会导致另一种情况，或者两者是否都是另一个过程的结果。实验证据表明，胰岛素抵抗和NAFLD均源于慢性炎症状态。驱动这种慢性炎症的机制尚不清楚，但可能包括肠道细菌产物进入门静脉血、肝脏和体循环，从而在遗传易感个体中引发持续的炎性细胞因子反应。需要更多的研究来评估这一假设，并确定中断这一致病级联反应的治疗方法的益处。
