Peluso Ilaria, Palmery Maura
Center of Nutrition, Council for Agricultural Research and Economics (CREA-NUT), Via Ardeatina 546, 00178 Rome, Italy.
Department of Physiology and Pharmacology "V. Erspamer", "Sapienza" University of Rome, P.le Aldo Moro 5, 00185 Rome, Italy.
Hum Immunol. 2016 Jan;77(1):47-53. doi: 10.1016/j.humimm.2015.10.008. Epub 2015 Oct 22.
Obesity is associated with many pathological conditions. Tumor Necrosis Factor-α (TNF-α) is one of the key mediators of inflammation involved in the obesity-related insulin resistance development. We aim to review the human evidence useful to clarify the relationship between inflammation and body weight, with particular reference to TNF-α. Genetic polymorphisms and epigenetic factors, such as diet, could affect TNF-α activity. TNF-α is associated with obesity, but also with anorexia and cachexia. Despite the role of TNF-α in obesity-related diseases, anti-TNF-α antibody therapy is associated with an increase in adiposity. In conclusion the reviewed results suggest that inflammation is more likely a consequence rather than a cause of obesity.
肥胖与许多病理状况相关。肿瘤坏死因子-α(TNF-α)是参与肥胖相关胰岛素抵抗发展的炎症关键介质之一。我们旨在综述有助于阐明炎症与体重之间关系的人体证据,尤其涉及TNF-α。基因多态性和表观遗传因素,如饮食,可能影响TNF-α活性。TNF-α与肥胖相关,但也与厌食和恶病质相关。尽管TNF-α在肥胖相关疾病中起作用,但抗TNF-α抗体治疗却与肥胖增加有关。总之,综述结果表明炎症更可能是肥胖的结果而非原因。