Ectopic Fat, Insulin Resistance, and Nonalcoholic Fatty Liver Disease Implications for Cardiovascular Disease
Ectopic Fat, Insulin Resistance, and Nonalcoholic Fatty Liver Disease Implications for Cardiovascular Disease
复制标题
异位脂肪、胰岛素抵抗和非酒精性脂肪肝对心血管疾病的影响
DOI：
10.1161/atvbaha.114.303034
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发表时间：
2014-06-01
影响因子：
8.7
通讯作者：
Targher, Giovanni
中科院分区：
文献类型：
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作者：
Byrne, Christopher D.;Targher, Giovanni
肝脏异位脂肪堆积导致非酒精性脂肪性肝病(NAFLD)，这是西方国家慢性肝病最常见的原因。异位肝脂，尤其是甘油二酯，会加剧肝脏胰岛素抵抗，促进全身炎症，增加患2型糖尿病和心血管疾病的风险。越来越多的证据表明，NAFLD是心血管疾病的一个新的危险因素，尽管目前没有获得批准的NAFLD本身的治疗方法，但目前的证据表明，他汀类药物治疗NAFLD是安全的。目前，没有足够的证据表明他汀类药物或其他心脏保护剂，如血管紧张素受体阻滞剂，在治疗NAFLD方面是有效的。在这篇简短的叙述性综述中，我们讨论了NAFLD的诊断以及异位肝脂肪在导致胰岛素抵抗和增加2型糖尿病和心血管疾病风险方面的作用。在这篇综述中，使用关键词非酒精性脂肪肝或脂肪肝合并糖尿病风险、心血管风险和心血管死亡率来搜索PubMed在1990至2014年间的文章。用英语以外的语言发表的文章被排除在外。
Ectopic fat accumulation in the liver causes nonalcoholic fatty liver disease (NAFLD), which is the most common cause of chronic liver disease in Western countries. Ectopic liver lipid, particularly diacylglycerol, exacerbates hepatic insulin resistance, promotes systemic inflammation, and increases risk of developing both type 2 diabetes mellitus and cardiovascular disease. Increasing evidence suggests that NAFLD is an emerging risk factor for cardiovascular disease, and although there are currently no licensed treatments for NAFLD per se, current evidence suggests that statin treatment is safe in NAFLD. Presently, there is insufficient evidence to indicate that statins or other cardioprotective agents, such as angiotensin receptor blockers, are effective in treating NAFLD. In this brief narrative review, we discuss the diagnosis of NAFLD and the role of ectopic liver fat to cause insulin resistance and to increase risk of both type 2 diabetes mellitus and cardiovascular disease. For this review, PubMed was searched for articles using the key words non-alcoholic fatty liver disease or fatty liver combined with diabetes risk, cardiovascular risk, and cardiovascular mortality between 1990 and 2014. Articles published in languages other than English were excluded.