Trail Receptor Deletion in Mice Suppresses the Inflammation of Nutrient Excess

摘要: Background & Aims Low-grade chronic inflammation is a cardinal feature of the metabolic syndrome, yet its pathogenesis not well defined. The purpose this study was to examine role TRAIL receptor (TR) signaling in obesity-associated using mice with genetic deletion TR. Methods TR knockout ( −/− ) and their littermate wild-type (WT) were fed diet high saturated fat, cholesterol fructose (FFC) or chow. Metabolic phenotyping, liver injury, adipose tissue assessed. Chemotaxis activation mouse bone marrow-derived macrophages (BMDMϕ) measured. Results Genetic completely repressed weight gain, adiposity insulin resistance FFC-fed mice. Moreover, suppressed steatohepatitis, essentially normal serum ALT, hepatocyte apoptosis triglyceride accumulation. Gene array data implicated inhibition macrophage-associated hepatic absence In keeping this, there diminished accumulation inflammatory tissue. BMDMϕ manifest reduced chemotaxis nuclear factor-κ B upon by palmitate lipopolysaccharide. Conclusions These advance concept that nutrient excess requires signaling.