Department of Biochemistry (U38-FCT), Faculty of Medicine, University of Porto, Al. Prof. Hernâni Monteiro, 4200-319 Porto, Portugal.
Mediators Inflamm. 2010;2010. doi: 10.1155/2010/289645. Epub 2010 Jul 14.
The increasing incidence of obesity and the metabolic syndrome is disturbing. The activation of inflammatory pathways, used normally as host defence, reminds the seriousness of this condition. There is probably more than one cause for activation of inflammation. Apparently, metabolic overload evokes stress reactions, such as oxidative, inflammatory, organelle and cell hypertrophy, generating vicious cycles. Adipocyte hypertrophy, through physical reasons, facilitates cell rupture, what will evoke an inflammatory reaction. Inability of adipose tissue development to engulf incoming fat leads to deposition in other organs, mainly in the liver, with consequences on insulin resistance. The oxidative stress which accompanies feeding, particularly when there is excessive ingestion of fat and/or other macronutrients without concomitant ingestion of antioxidant-rich foods/beverages, may contribute to inflammation attributed to obesity. Moreover, data on the interaction of microbiota with food and obesity brought new hypothesis for the obesity/fat diet relationship with inflammation. Beyond these, other phenomena, for instance psychological and/or circadian rhythm disturbances, may likewise contribute to oxidative/inflammatory status. The difficulty in the management of obesity/metabolic syndrome is linked to their multifactorial nature where environmental, genetic and psychosocial factors interact through complex networks.
肥胖症和代谢综合征发病率的上升令人不安。炎症途径的激活,通常被用作宿主防御,提醒人们这种情况的严重性。炎症的激活可能不止一个原因。显然,代谢超负荷会引发应激反应,如氧化、炎症、细胞器和细胞肥大,产生恶性循环。脂肪细胞肥大通过物理原因促进细胞破裂,从而引发炎症反应。脂肪组织发展不能吞噬摄入的脂肪,导致脂肪在其他器官沉积,主要在肝脏,导致胰岛素抵抗。进食时伴随的氧化应激,特别是当过量摄入脂肪和/或其他宏量营养素而没有同时摄入富含抗氧化剂的食物/饮料时,可能会导致肥胖相关的炎症。此外,关于微生物群与食物和肥胖相互作用的数据为肥胖/脂肪饮食与炎症之间的关系提供了新的假设。除此之外,其他现象,例如心理和/或昼夜节律紊乱,也可能导致氧化/炎症状态。肥胖症/代谢综合征的治疗困难与它们的多因素性质有关,环境、遗传和社会心理因素通过复杂的网络相互作用。