Acute necrotizing pancreatitis induces lipidosis

Objective To examine changes in lipid metabolism in acute necrotizing pancreatitis (ANP) and its influence on inflammation. Methods Thirty six SD rats were equally randomized into six groups: control group, and 3 h, 6 h, 12 h, 24 h and 48 h ANP groups. Rats in the ANP groups were injected with 5% sodium taurocholate into the bioliopancreatic duct to induce an ANP model, and then sacrificed at 3 h, 6 h, 12 h, 24 h and 48 h after ANP. By light microscopy and electron microscopy, severity of pancreatitis was assessed using a histological scoring system, and histopathologic damage to the pancreas was observed. Serum amylase, cholesterin, triacylglycerol (TG), free fatty acid (FFA) and lipoprotein lipase (LPL) levels were determined. SCD1 and CD36 mRNA were measured by RT-PCR. Results The Amy values and the scores of the pancreatic histopathology system in ANP groups were the highest at 12 h of ANP. Electron microscopy showed that ANP induced mild endoplasmic reticulum dilatation and increase in zymogen granules. Serum TG and FFA values were higher in ANP groups than those in the control group; especially serum TG of the 24-h ANP group was significantly higher than that of the control [0.81 ± 0.35 vs 0.39 ± 0.22, P 0.01]. Serum FFA value of the 6-h ANP group was significantly higher than that of the control [1.32 ± 0.32 vs 0.89 ± 0.14, P 0.05]. Serum LPL activity was lower in ANP rats. SCD1, CD36 mRNA expression was increased in ANP rats. Conclusions Hyperlipidemia, abnormal expression of lipid metabolism-related enzymes and dilation of endoplasmic reticulum of pancreatic acini were observed in ANP, suggesting that ANP may induce lipidosis.