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饮食因素与低度炎症与超重和肥胖的关系。

Dietary factors and low-grade inflammation in relation to overweight and obesity.

机构信息

School of Medicine, University of Southampton, Southampton, UK.

出版信息

Br J Nutr. 2011 Dec;106 Suppl 3:S5-78. doi: 10.1017/S0007114511005460.

Abstract

Low-grade inflammation is a characteristic of the obese state, and adipose tissue releases many inflammatory mediators. The source of these mediators within adipose tissue is not clear, but infiltrating macrophages seem to be especially important, although adipocytes themselves play a role. Obese people have higher circulating concentrations of many inflammatory markers than lean people do, and these are believed to play a role in causing insulin resistance and other metabolic disturbances. Blood concentrations of inflammatory markers are lowered following weight loss. In the hours following the consumption of a meal, there is an elevation in the concentrations of inflammatory mediators in the bloodstream, which is exaggerated in obese subjects and in type 2 diabetics. Both high-glucose and high-fat meals may induce postprandial inflammation, and this is exaggerated by a high meal content of advanced glycation end products (AGE) and partly ablated by inclusion of certain antioxidants or antioxidant-containing foods within the meal. Healthy eating patterns are associated with lower circulating concentrations of inflammatory markers. Among the components of a healthy diet, whole grains, vegetables and fruits, and fish are all associated with lower inflammation. AGE are associated with enhanced oxidative stress and inflammation. SFA and trans-MUFA are pro-inflammatory, while PUFA, especially long-chain n-3 PUFA, are anti-inflammatory. Hyperglycaemia induces both postprandial and chronic low-grade inflammation. Vitamin C, vitamin E and carotenoids decrease the circulating concentrations of inflammatory markers. Potential mechanisms are described and research gaps, which limit our understanding of the interaction between diet and postprandial and chronic low-grade inflammation, are identified.

摘要

低度炎症是肥胖状态的一个特征,脂肪组织释放许多炎症介质。这些介质在脂肪组织中的来源尚不清楚,但浸润的巨噬细胞似乎尤为重要,尽管脂肪细胞本身也发挥作用。肥胖者的许多炎症标志物的循环浓度高于瘦者,这些标志物被认为在引起胰岛素抵抗和其他代谢紊乱方面发挥作用。减肥后,血液中炎症标志物的浓度降低。在用餐数小时后,血液中炎症介质的浓度升高,在肥胖者和 2 型糖尿病患者中更为明显。高糖和高脂肪膳食均可引起餐后炎症,膳食中晚期糖基化终产物(AGE)含量高会加重这种炎症,而膳食中包含某些抗氧化剂或含抗氧化剂的食物则会部分减轻这种炎症。健康的饮食模式与较低的循环炎症标志物浓度相关。在健康饮食的组成部分中,全谷物、蔬菜和水果以及鱼类均与较低的炎症相关。AGE 与增强的氧化应激和炎症相关。饱和脂肪酸(SFA)和反式单不饱和脂肪酸(trans-MUFA)具有促炎作用,而多不饱和脂肪酸(PUFA),尤其是长链 n-3 PUFA,具有抗炎作用。高血糖诱导餐后和慢性低度炎症。维生素 C、维生素 E 和类胡萝卜素可降低循环炎症标志物的浓度。描述了潜在机制,并确定了研究空白,这些空白限制了我们对饮食与餐后和慢性低度炎症相互作用的理解。

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