tailieunhanh - Báo cáo y học: "Inflammatory Signals shift from adipose to liver during high fat feeding and influence the development of steatohepatitis in mice"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Inflammatory Signals shift from adipose to liver during high fat feeding and influence the development of steatohepatitis in mice. | Stanton et al. Journal of Inflammation 2011 8 8 http content 8 1 8 JOURNAL OF INFLAMMATION RESEARCH Open Access Inflammatory Signals shift from adipose to liver during high fat feeding and influence the development of steatohepatitis in mice 1 2 1 1 - Michaela C Stanton Shu-Cheng Chen James V Jackson Alberto Rojas-Triana David Kinsley Long Cui Jay S Fine2 3 Scott Greenfeder1 Loretta A Bober1 Chung-Her Jenh1 Abstract Background Obesity and inflammation are highly integrated processes in the pathogenesis of insulin resistance diabetes dyslipidemia and non-alcoholic fatty liver disease. Molecular mechanisms underlying inflammatory events during high fat diet-induced obesity are poorly defined in mouse models of obesity. This work investigated gene activation signals integral to the temporal development of obesity. Methods Gene expression analysis in multiple organs from obese mice was done with Taqman Low Density Array TLDA using a panel of 92 genes representing cell markers cytokines chemokines metabolic and activation genes. Mice were monitored for systemic changes characteristic of the disease including hyperinsulinemia body weight and liver enzymes. Liver steatosis and fibrosis as well as cellular infiltrates in liver and adipose tissues were analyzed by histology and immunohistochemistry. Results Obese C57BL 6 mice were fed with high fat and cholesterol diet HFC for 6 16 and 26 weeks. Here we report that the mRNA levels of macrophage and inflammation associated genes were strongly upregulated at different time points in adipose tissues 6-16 weeks and liver 16-26 weeks after the start of HFC feeding. CD11b and CD11c macrophages highly infiltrated HFC liver at 16 and 26 weeks. We found clear evidence that signals for IL-1Ị3 IL1RN TNF-a and TGFp-1 are present in both adipose and liver tissues and that these are linked to the development of inflammation and insulin resistance in the HFC-fed mice. Conclusions Macrophage infiltration .