Ferrante A W
Naomi Berrie Diabetes Center, Columbia University, New York, NY 10032, USA.
J Intern Med. 2007 Oct;262(4):408-14. doi: 10.1111/j.1365-2796.2007.01852.x.
Obesity induces an inflammation state that is implicated in many clinically important complications, including insulin resistance, diabetes, atherosclerosis and non-alcoholic fatty liver disease. Although the cause and the molecular participants in this process remain incompletely defined, adipose tissue has a central role. Obesity-induced production of pro-inflammatory molecules, typified by TNF-alpha was recognized more than a dozen years ago, and since then more than two dozen other pro-inflammatory molecules induced by obesity have been identified. More recently a critical role for immune cells, specifically mononuclear phagocytes, in generating the obesity-induced inflammation has been identified. Defining the molecular and cellular components of obesity-induced inflammation offers the potential of identifying therapeutic targets that can ameliorate the complications associated with obesity.
肥胖会引发一种炎症状态，这种状态与许多临床上重要的并发症相关，包括胰岛素抵抗、糖尿病、动脉粥样硬化和非酒精性脂肪性肝病。尽管这一过程的病因和分子参与者仍未完全明确，但脂肪组织起着核心作用。肥胖诱导产生的促炎分子，以肿瘤坏死因子-α为代表，早在十几年前就已被认识到，从那时起，又发现了二十多种由肥胖诱导产生的其他促炎分子。最近，已确定免疫细胞，特别是单核吞噬细胞，在引发肥胖诱导的炎症中起关键作用。明确肥胖诱导炎症的分子和细胞成分，为识别可改善与肥胖相关并发症的治疗靶点提供了可能性。
