Insulin-Like Growth Factor-1 Deficiency and Cirrhosis Establishment

Rocio G. de la Garza, Luis Alonso Morales-Garza, Irene Martin-Estal, Inma Castilla-Cortazar

Abstract


Cirrhosis represents the final stage of chronic liver damage, which can be due to different factors such as alcohol, metabolic syndrome with liver steatosis, autoimmune diseases, drugs, toxins, and viral infection, among others. Nowadays, cirrhosis is an important health problem and it is an increasing cause of morbidity and mortality, being the 14th most common cause of death worldwide. The physiopathological pathways that lead to fibrosis and finally cirrhosis partly depend on the etiology. Nevertheless, some common features are shared in this complex mechanism. Recently, it has been demonstrated that cirrhosis is a dynamic process that can be altered in order to delay or revert fibrosis. In addition, when cirrhosis has been established, insulin-like growth factor-1 (IGF-1) deficiency or reduced availability is a common condition, independently of the etiology of chronic liver damage that leads to cirrhosis. IGF-1 deprivation seriously contributes to the progressive malnutrition of cirrhotic patient, increasing the vulnerability of the liver to establish an inflammatory and oxidative microenvironment with mitochondrial dysfunction. In this context, IGF-1 deficiency in cirrhotic patients can justify some of the common characteristics of these individuals. Several studies in animals and humans have been done in order to test the replacement of IGF-1 as a possible therapeutic option, with promising results.




J Clin Med Res. 2017;9(4):233-247
doi: https://doi.org/10.14740/jocmr2761w


Keywords


IGF-1; Steatosis; Non-alcoholic fatty liver disease; Acute liver damage; GH/IGF-1 axis; Fibrogenesis; Oxidative damage; Mitochondrial protection

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