Regulation of diseases by chronic inflammation and obesity

众所周知，肥胖可通过诱导慢性炎症加重代谢综合征和糖耐量。我们已经建立了p38α突变小鼠，其中p38α基因在造血细胞中被破坏。结果发现，高脂饮食诱导的脂肪组织慢性炎症和糖耐量均有改善，提示造血细胞中的p38α信号通路可能参与了肥胖诱导的慢性炎症和代谢综合征的调节。

It is well established that obesity can exacerbate metabolic syndrome and glucose tolerance through induction of chronic inflammation. We have established p38alpha mutant mice in which p38alpha gene is disrupted in the hematopoietic cells. It is found that high fat diet-induced chronic inflammation in the adipose tissue and glucose tolerance is ameliorated in the mutant mice, suggesting that the p38alpha signaling cascade in the hematopoietic cells could be involved in the regulation of obesity-induced chronic inflammation and metabolic syndrome.