Department of Immunology, Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, Iran.
Institute of Immunology, University of Kiel, Kiel, Germany.
Scand J Immunol. 2019 Apr;89(4):e12747. doi: 10.1111/sji.12747. Epub 2019 Jan 29.
Obesity is associated with chronic low-grade inflammation of the adipose tissue (AT) that might develop into systemic inflammation, insulin resistance (IR) and an increased risk of type 2 diabetes mellitus (T2DM) in severe obese rodents and humans. In the lean state, small normal adipocytes and AT macrophages interact with each other to maintain metabolic homeostasis but during obesity, enlarged adipocytes secrete inflammatory mediators and express immune receptors to recruit immune cells and aggravate the inflammation. The better understanding of the obesity-related inflammatory milieu and the sequential events leading to IR could be helpful in designing new preventive and therapeutic strategies. The present review will discuss the cellular and molecular abnormalities participating in the pathogenesis of obesity in obese individuals as well as high-fat diet (HFD)-fed mice, a mouse model of obesity.
肥胖与脂肪组织(AT)的慢性低度炎症有关,这种炎症可能发展为全身性炎症、胰岛素抵抗(IR),并增加肥胖啮齿动物和人类患 2 型糖尿病(T2DM)的风险。在正常状态下,小的正常脂肪细胞和 AT 巨噬细胞相互作用以维持代谢平衡,但在肥胖时,增大的脂肪细胞会分泌炎症介质并表达免疫受体,招募免疫细胞并加重炎症。更好地了解肥胖相关的炎症环境以及导致 IR 的连续事件,可能有助于设计新的预防和治疗策略。本综述将讨论参与肥胖个体以及高脂肪饮食(HFD)喂养的肥胖小鼠发病机制的细胞和分子异常,肥胖小鼠模型。