Macías-Rodríguez Ricardo Ulises, Torre Aldo
Departamento de Gastroenterología del Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, México D.F.
Rev Invest Clin. 2009 Mar-Apr;61(2):161-72.
Cryptogenic cirrhosis represents the third cause of cirrhosis in Mexico and comprises the clinical spectrum of NAFLD. Insulin resistance is the main factor in NASH development, as well as genetic and environmental factors. Derangement in insulin signaling pathways, either pre-receptor or post-receptor, causes insulin resistance (IR). The post-receptor dysfunction represents the primary cause of IR and links with metabolic syndrome, mainly diabetes and obesity. Prevailing metabolic moment will establish the IR status. NASH progression causes fibrosis, cirrhosis and hepatocelular carcinoma. Therapy is currently directed at treating components of the metabolic syndrome which may be beneficial for the liver. Through different mechanisms IR originates to fat deposit in liver and subsequently under oxidative stress and pro-inflammatory cytokines and then to inflammatory infiltrate, fibrosis and finally cirrhosis. This review focuses on insulin resistance and the related mechanisms of hepatic damage.
隐源性肝硬化是墨西哥肝硬化的第三大病因，涵盖了非酒精性脂肪性肝病（NAFLD）的临床谱系。胰岛素抵抗是NASH发生发展的主要因素，此外还有遗传和环境因素。胰岛素信号通路在受体前或受体后的紊乱都会导致胰岛素抵抗（IR）。受体后功能障碍是IR的主要原因，并与代谢综合征相关，主要是糖尿病和肥胖。占主导地位的代谢状态将决定IR的状况。NASH的进展会导致纤维化、肝硬化和肝细胞癌。目前的治疗旨在针对代谢综合征的组成部分，这可能对肝脏有益。通过不同机制，IR导致脂肪在肝脏中沉积，随后在氧化应激和促炎细胞因子作用下，进而引发炎症浸润、纤维化，最终发展为肝硬化。本综述聚焦于胰岛素抵抗及肝损伤的相关机制。
