Resistin In Mice With Hepatic Lipid Deposition Induced By Chronic Inflammation

Objective: To examine the expression and secretion of resistin in micewith hepatic lipid deposition induced by chronic inflammation.Methods: Casein was injected in C57BL/6J mice to induce a chronicsystemic inflammatory stress in vivo. Serum was analyzed for inflammatorycytokines, resistin, insulin and free fatty acid. Liver was taken for Oil Red Ostaining and lipid analysis. Insulin sensitivity was evaluated by insulintolerance tests. Real-time polymerase chain reaction was used to examinethe gene expression of resistin and molecules involved in lipid metabolism.Results: Casein injection elevated serum levels of inflammatorycytokines (eg. serum amyloid A protein, interleukin-6, tumor necrosis factorα, monocyte chemoattractant protein-1) in mice (P<0.01), increased lipidaccumulation in liver (P<0.05) and induced smaller lipid droplets in adiposetissue. Inflammation increased serum fasting insulin and free fatty acidlevels and induced insulin resistance in C57BL/6J mice (P<0.05). Theinflammatory stress inhibited mRNA expression of carnitine palmitoyltransferase, acyl-coenzyme A oxidase1, microsomal triacylglycerol transferprotein in liver (P<0.05), suggesting that chronic systemic inflammation induces liver lipid metabolism disorders. The mRNA expression of resistinwas up-regulated in epididymal adipose tissues (P<0.05) and an increasedtendency in liver and the serum level of resistin was increased ininflammatory group (P=0.008, P=0.001).Conclusion: Epididymal fat resistin expression and serum level areelevated in mice with hepatic lipid deposition induced by chronicinflammation, suggesting that resistin may play an important role in liverlipid deposition which induced by chronic inflammation.