fig1

Figure 1. Summary of results and outcomes. The study by Dodig et al.^[12] investigates the role of insulin in enhancing type I collagen synthesis in primary HSC cultures under high glucose conditions. Insulin treatment significantly increased type I collagen promoter activity and protein levels, particularly at 5 μM, without affecting HSC proliferation. The effects were independent of PI3 kinase signaling despite AKT phosphorylation indicating active pathway engagement. Insulin also promoted HSC adhesion to fibronectin and elevated α5β1 integrin and phosphorylated FAK levels. Knocking down α5 integrin reduced collagen synthesis and inhibited insulin’s effects on both α5 integrin and collagen levels. In vivo analysis of L-SACC1 transgenic mice showed increased ECM deposition and enhanced type I collagen production by isolated HSCs compared to wild-type controsls. ECM: Extracellular matrix; FAK: focal adhesion kinase; HSC: hepatic stellate cell; WT: wild-type.