ESPE2016 Free Communications Pathophysiology of Obesity (6 abstracts)
Background: Type 1 insulin-like growth factor receptor (IGF-1R) is the product of a single-copy gene located on chromosome 15 and is ubiquitously expressed in humans. Increased hepatic IGF-1R gene expression is found in hepatocellular carcinoma and in chronic hepatitis C, making parenchymal and non-parenchymal cells more susceptible to the mitogenic effects of IGF-1.
Objective and hypotheses: As we have previously demonstrated that IGF-1 and IGF-2 circulating levels are rearranged in relation with the severity of liver damage in obese children with NAFLD, our aim was to investigate the hepatic expression of IGF-1R in the same group of patients.
Method: In this preliminary study, immunohistochemistry and immunofluorescence were applied for analysing the expression of IGF-1R in 12 children with NAFLD. Three liver samples from healthy subjects were used as reference for tissue expression of IGF-1R. Expression data were correlated with severity of disease and with the expression of various liver cell markers.
Results: Tissue expression of IGF-1R in liver samples from children with NAFLD is highly variable and expressed in both parenchymal and non-parenchymal cells. IGF-1R expression is strongly correlated with the severity of inflammation and fibrosis, decreasing in parallel to NAFLD activity score and increasing in patients with moderate to severe degree of fibrosis. Finally, the IGF-1R expression correlated with the number of hepatic stellate cells.
Conclusion: Our preliminary data suggest that IGF-1R expression in liver is strongly related with the severity of fibrosis, suggesting, for the first time, that IGF-1R may play a role in the regulation of hepatic regeneration induced by liver fibrosis in obese children with NAFLD.
10 Sep 2016 - 12 Sep 2016