Department of Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Minerva Foundation Institute for Medical Research, Helsinki, Finland.
Diabetologia. 2024 Jun;67(6):961-973. doi: 10.1007/s00125-024-06087-7. Epub 2024 Feb 9.
Fatty liver plays a pivotal role in the pathogenesis of the metabolic syndrome and type 2 diabetes. According to an updated classification, any individual with liver steatosis and one or more features of the metabolic syndrome, without excess alcohol consumption or other known causes of steatosis, has metabolic dysfunction-associated steatotic liver disease (MASLD). Up to 60-70% of all individuals with type 2 diabetes have MASLD. However, the prevalence of advanced liver fibrosis in type 2 diabetes remains uncertain, with reported estimates of 10-20% relying on imaging tests and likely overestimating the true prevalence. All stages of MASLD impact prognosis but fibrosis is the best predictor of all-cause and liver-related mortality risk. People with type 2 diabetes face a two- to threefold increase in the risk of liver-related death and hepatocellular carcinoma, with 1.3% progressing to severe liver disease over 7.7 years. Because reliable methods for detecting steatosis are lacking, MASLD mostly remains an incidental finding on imaging. Regardless, several medical societies advocate for universal screening of individuals with type 2 diabetes for advanced fibrosis. Proposed screening pathways involve annual calculation of the Fibrosis-4 (FIB-4) index, followed by a secondary test such as transient elastography (TE) for intermediate-to-high-risk individuals. However, owing to unsatisfactory biomarker specificity, these pathways are expected to channel approximately 40% of all individuals with type 2 diabetes to TE and 20% to tertiary care, with a false discovery rate of up to 80%, raising concerns about feasibility. There is thus an urgent need to develop more effective strategies for surveying the liver in type 2 diabetes. Nonetheless, weight loss through lifestyle changes, pharmacotherapy or bariatric surgery remains the cornerstone of management, proving highly effective not only for metabolic comorbidities but also for MASLD. Emerging evidence suggests that fibrosis biomarkers may serve as tools for risk-based targeting of weight-loss interventions and potentially for monitoring response to therapy.
脂肪肝在代谢综合征和 2 型糖尿病的发病机制中起着关键作用。根据最新分类，任何有肝脂肪变性和代谢综合征的一个或多个特征的个体，没有过量饮酒或其他已知的脂肪变性原因，都有代谢功能相关的脂肪性肝病（MASLD）。高达 60-70%的 2 型糖尿病患者都有 MASLD。然而，2 型糖尿病患者中晚期肝纤维化的患病率仍不确定，据报道，依赖影像学检查的估计值为 10-20%，可能高估了真实患病率。MASLD 的所有阶段都影响预后，但纤维化是所有原因和肝脏相关死亡率风险的最佳预测因素。2 型糖尿病患者的肝脏相关死亡和肝细胞癌风险增加 2-3 倍，其中 1.3%的患者在 7.7 年内进展为严重肝病。由于缺乏可靠的检测脂肪变性的方法，MASLD 大多只是影像学检查的偶然发现。尽管如此，一些医学协会还是主张对 2 型糖尿病患者进行晚期纤维化的普遍筛查。建议的筛查途径包括每年计算纤维化 4 指数（FIB-4 指数），然后对中高危人群进行瞬时弹性成像（TE）等二级检测。然而，由于生物标志物特异性不理想，这些途径预计将使大约 40%的 2 型糖尿病患者接受 TE 检查，20%的患者接受三级护理，假阳性率高达 80%，这引起了对可行性的担忧。因此，迫切需要开发更有效的策略来调查 2 型糖尿病患者的肝脏情况。尽管如此，通过生活方式改变、药物治疗或减肥手术减轻体重仍然是管理的基石，这不仅对代谢合并症有效，而且对 MASLD 也有效。新出现的证据表明，纤维化生物标志物可以作为基于风险的减肥干预措施的靶向工具，并可能用于监测对治疗的反应。
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