Figure 2.

Proposed mechanisms of action of docosahexaenoic acid (DHA) in hypertriglyceridemic and hyperlipidemic acute pancreatitis. DHA inhibits triglyceride (TG) and fatty acid (FA) synthesis in the liver. DHA increases lipoprotein lipase (LPL) activity in the extrahepatic tissues and β-oxidation of FA in the liver and skeletal muscles, thereby contributing to the reduction of FA delivery to the liver and reducing plasma TG levels. High amounts of FAs induce pancreatic inflammation and injury. Therefore, the TG-lowering effect of DHA may prevent hypertriglyceridemic acute pancreatitis. On the other hand, a high concentration of DHA increases Ca²⁺ and activates PKC isoforms (PKC-α, PKC-δ, PKC-ε, and PKC-ζ) in pancreatic acinar cells, which may induce zymogene activation and pancreatic injury associated with hyperlipidemic acute pancreatitis. In addition, PKC activates NF-κB and induces inflammatory cytokine expression in pancreatic acinar cells. The bars represent inhibition, while the arrows represent stimulation.