Khatib Subreen A, Rossi Emily L, Bowers Laura W, Hursting Stephen D
Department of Nutrition, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States.
Prostaglandins Other Lipid Mediat. 2016 Sep;125:100-7. doi: 10.1016/j.prostaglandins.2016.07.011. Epub 2016 Jul 19.
Today's world population has an unprecedented risk of dying from the consequences of being overweight and obese. Chronic diseases such as cardiovascular disease, type 2 diabetes, and cancer are often accelerated because of excessive adiposity. Various biological mechanisms are implicated in the obesity-cancer link, particularly local and systemic inflammation as well as altered growth factor signaling pathways. In order to combat obesity-induced inflammation and the resulting increases in cancer risk and progression, the identification of safe and effective mechanism-based interventions is imperative. Notably, long chain omega-3 polyunsaturated fatty acids (PUFAs) modulate the secretion of pro-inflammatory cytokines, prostaglandins and other inflammatory mediators, restore insulin sensitivity, and can prevent or delay tumorigenesis. Delineating the precise mechanisms by which omega-3 PUFAs suppress obesity-induced inflammation will help identify promising key mechanistic targets and intervention strategies to break the obesity-cancer link.
当今世界人口因超重和肥胖而面临前所未有的死亡风险。诸如心血管疾病、2型糖尿病和癌症等慢性疾病常常因过度肥胖而加速发展。肥胖与癌症之间的联系涉及多种生物学机制,特别是局部和全身炎症以及生长因子信号通路的改变。为了对抗肥胖引发的炎症以及由此导致的癌症风险增加和病情进展,识别基于机制的安全有效的干预措施势在必行。值得注意的是,长链ω-3多不饱和脂肪酸(PUFAs)可调节促炎细胞因子、前列腺素和其他炎症介质的分泌,恢复胰岛素敏感性,并能预防或延缓肿瘤发生。阐明ω-3多不饱和脂肪酸抑制肥胖诱导炎症的确切机制,将有助于识别有前景的关键机制靶点和干预策略,以打破肥胖与癌症之间的联系。