Pathophysiologic role of saturated fatty acids in the metabolic syndrome

饱和脂肪酸的过量生产被认为是代谢综合征的分子基础。在这项研究中，我们专注于肥胖脂肪组织中脂肪细胞和巨噬细胞之间的亲密串扰，并确定抗炎转录因子ATF3和结核分枝杆菌的病原体传感器Mincle是脂肪组织炎症的新调节因子。因此，肥胖时肥大的脂肪细胞大量释放的饱和脂肪酸可能会导致脂肪组织的炎性变化，以及肝脏和骨骼肌等远处器官的脂毒性。

Overproduction of saturated fatty acids is considered to be a molecular basis of the metabolic syndrome. In this study, we focused on the intimate crosstalk between adipocytes and macrophages in obese adipose tissue and identified ATF3, an anti-inflammatory transcriptionfactor, and Mincle, a pathogen sensor for mycobacterium tuberculosis, as novel regulators of adipose tissue inflammation. Thus, saturated fatty acids, which are released abundantly from hypertrophied adipocytes in obesity, may induce inflammatory changes in adipose tissue as well as lipotoxicity in remote organs such as liver and skeletal muscle.