Molecular and Cellular Biology Program, Ohio University , Athens , OH , USA.
Biomedical Engineering Program, Russ College of Engineering and Technology, Ohio University , Athens , OH , USA.
Int Rev Immunol. 2019;38(4):157-171. doi: 10.1080/08830185.2019.1638921. Epub 2019 Jul 9.
Obesity predisposes the affected individuals to several metabolic, inflammatory, cardiovascular and malignant pathologies and is a top risk factor for premature mortality. It is now well known that inflammation has a major causative role in obesity-associated disease development and that obesity favors the establishment of a pro-inflammatory milieu at the level of adipose microenvironment. These inflammatory signals result in a disruption of normal cellular-crosstalk between adipose and non-adipose components leading to an altered metabolic and immunological status and a dysfunctional phenotype. Abnormal secretion of adipokines - small adipose-derived signaling molecules - can further assist in the inflammatory processes to offset the adipose tissue towards a dysfunctional state. Although adipokines have been recognized as the link between obesity and pathogenesis, studies are needed to fully understand their mechanism of action and underscore their therapeutic value. Here, we have reviewed obesity-induced metabolic and immunological changes at the level of vasculature and emphasize on the importance of adipokines, particularly leptin, vaspin and visfatin, for their therapeutic relevance.
肥胖使受影响的个体易患多种代谢、炎症、心血管和恶性疾病，是导致过早死亡的首要危险因素。现在众所周知，炎症在肥胖相关疾病的发展中起着主要的致病作用，肥胖有利于在脂肪微环境水平建立促炎环境。这些炎症信号导致脂肪组织与非脂肪成分之间正常的细胞串扰中断，导致代谢和免疫状态改变以及功能障碍表型。脂肪细胞因子的异常分泌 - 小的脂肪衍生信号分子 - 可以进一步协助炎症过程，使脂肪组织向功能障碍状态发展。尽管脂肪细胞因子已被认为是肥胖与发病机制之间的联系，但仍需要进一步的研究来充分了解它们的作用机制，并强调它们的治疗价值。在这里，我们综述了肥胖诱导的血管水平的代谢和免疫变化，并强调了脂肪细胞因子（特别是瘦素、vaspin 和 visfatin）的重要性，因为它们具有治疗相关性。
