肥胖和代谢综合征相关机制和研究进展

Mechanisms and Research Progress Relatedto Obesity and Metabolic Syndrome

肥胖症和代谢综合征(Metabolic syndrome, MetS)的发病率正在不断上升,炎症通路的激活通常被用作是宿主的一种防御手段,提醒人们该疾病的严重性。导致炎症激活的原因可能不止一个。代谢超负荷会引起应激反应,如氧化应激、炎症反应、细胞器和细胞肥大,从而产生恶性循环。脂肪细胞肥大会导致细胞破裂,从而引发炎症反应。脂肪组织的发育无法吞噬细胞破裂产生的脂肪,导致脂肪沉积在其他器官(主要是肝脏),从而诱发胰岛素抵抗。人们进食时也会产生氧化应激,尤其摄入过多的脂肪和/或其他营养素时却没有同时摄入富含抗氧化剂的食物的情况下,可能导致肥胖引起炎症。此外,有关微生物群与食物和肥胖相互作用的数据为肥胖/脂肪饮食与炎症的关系提出了新的假设。除此之外,其他现象,如心理和/或昼夜节律紊乱,也同样可能导致氧化/炎症状态。肥胖症/代谢综合征的治疗难度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。

The prevalence of obesity and Metabolic syndrome (MetS) is increasing, and the activation of in-flammatory pathways is often used as a host defense and a reminder of the severity of the disease. There may be more than one cause of inflammatory activation. Metabolic overload induces a vicious cycle of stress responses such as oxidative stress, inflammatory responses, and organelle and cellu-lar hypertrophy. Adipocyte hypertrophy leads to cellular rupture, which triggers an inflammatory response. The development of adipose tissue is unable to phagocytose the fat produced by cell rup-ture, leading to fat deposition in other organs (mainly the liver), thus inducing insulin resistance. Oxidative stress also occurs when people eat, especially if they consume too much fat and/or other nutrients without also consuming antioxidant-rich foods, which can lead to obesity-induced in-flammation. In addition, data on microbiota interactions with food and obesity suggest new hy-potheses for the relationship between obesity/fat diets and inflammation. In addition to this, other phenomena, such as psychological and/or circadian rhythm disturbances, may likewise contribute to the oxidative/inflammatory state. The difficulty in treating obesity/metabolic syndrome is re-lated to their multifactorial nature, where environmental, genetic and psychosocial factors interact through a complex network.