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住院肥胖的真实代价:肥胖对炎症应激和发病率的影响。

The true cost of in-patient obesity: impact of obesity on inflammatory stress and morbidity.

机构信息

Institute of Human Nutrition, DOHaD Division, School of Medicine, University of Southampton, Mailpoint 887, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK.

出版信息

Proc Nutr Soc. 2010 Nov;69(4):511-7. doi: 10.1017/S0029665110001709. Epub 2010 Jul 2.

Abstract

The objective of the present review is to provide an overview of the metabolic effects of pro-inflammatory cytokine production during infection and injury; to highlight the disadvantages of pro-inflammatory cytokine production and inflammatory stress on morbidity and mortality of patients; to identify the influence of genetics and adiposity on inflammatory stress in patients and to indicate how nutrients may modulate the inflammatory response in patients. Recent research has shown clearly that adipose tissue actively secretes a wide range of pro- and anti-inflammatory cytokines. Paradoxically, although inflammation is an essential part of the response of the body to infection, surgery and trauma, it can adversely affect patient outcome. The metabolic effects of inflammation are mediated by pro-inflammatory cytokines. Metabolic effects include insulin insensitivity, hyperlipidaemia, muscle protein loss and oxidant stress. These effects, as well as being present during infective disease, are also present in diseases with a covert inflammatory basis. These latter diseases include obesity and type 2 diabetes mellitus. Inflammatory stress also increases during aging. The level of cytokine production, within individuals, is influenced by single nucleotide polymorphisms (SNP) in cytokine genes. The combination of SNP controls the relative level of inflammatory stress in both overt and covert inflammatory diseases. The impact of cytokine genotype on the intensity of inflammatory stress derived from an obese state is unknown. While studies remain to be done in the latter context, evidence shows that these genomic characteristics influence morbidity and mortality in infectious disease and diseases with an underlying inflammatory basis and thereby influence the cost of in-patient obesity. Antioxidants and n-3 PUFA alter the intensity of the inflammatory process. Recent studies show that genotypic factors influence the effectiveness of immunonutrients. A better understanding of this aspect of nutrient-gene interactions and of the genomic factors that influence the intensity of inflammation during disease will help in the more effective targeting of nutritional therapy.

摘要

本综述的目的是概述感染和损伤时促炎细胞因子产生的代谢效应;强调促炎细胞因子产生和炎症应激对患者发病率和死亡率的不利影响;确定遗传和肥胖对患者炎症应激的影响,并指出营养素如何调节患者的炎症反应。最近的研究清楚地表明,脂肪组织积极分泌广泛的促炎和抗炎细胞因子。矛盾的是,尽管炎症是机体对感染、手术和创伤反应的重要组成部分,但它会对患者的预后产生不利影响。炎症的代谢效应是由促炎细胞因子介导的。代谢效应包括胰岛素抵抗、血脂异常、肌肉蛋白丢失和氧化应激。这些效应不仅存在于感染性疾病中,也存在于具有隐匿性炎症基础的疾病中。后者包括肥胖症和 2 型糖尿病。炎症应激也随着衰老而增加。个体细胞因子产生的水平受细胞因子基因中单核苷酸多态性(SNP)的影响。SNP 控制着显性和隐匿性炎症疾病中炎症应激的相对水平。细胞因子基因型对肥胖状态引起的炎症应激强度的影响尚不清楚。虽然在后一种情况下仍需要进行研究,但有证据表明,这些基因组特征影响感染性疾病和具有潜在炎症基础的疾病的发病率和死亡率,从而影响住院肥胖症的成本。抗氧化剂和 n-3PUFA 改变炎症过程的强度。最近的研究表明,基因型因素影响免疫营养素的有效性。更好地了解营养素-基因相互作用的这一方面以及影响疾病期间炎症强度的基因组因素将有助于更有效地针对营养治疗。

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