Abstract
Type 2 diabetes is a chronic metabolic disorder characterized, among other features, by elevated levels of circulatory free fatty acids. Several studies in animal and cellular models indicate that increased accumulation of lipids leads to oxidative and ER stress, mitochondrial dysfunction and alteration of proteostasis, resulting in cellular dysfunction. Proteostasis is mainly regulated by two pathways, the “ubiquitin-proteasome system” and the “autophagy-lysosomal system”. The proteolytic systems degrade un-/misfolded proteins and regulate the functional protein pool. However, it remains elusive if a hyperlipidemic environment leads to cellular dysfunction via alterations of both proteolytic systems. The purpose of this study is to investigate the role of the proteolytic systems in lipotoxic conditions. Therefore, we induced lipid accumulation in HepG2 cells by exposing them to palmitic acid. According to preliminary data palmitic acid induced lipid droplet formation and alters the cellular redox state, iNOS levels and induces ER stress. Under these conditions, further experiments are being performed to elucidate the impact of lipotoxic stress on the proteolytic systems in HepG2 cells.
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