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首页> 外文期刊>Proceedings of the Nutrition Society >The true cost of in-patient obesity: impact of obesity on inflammatory stress and morbidity.
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The true cost of in-patient obesity: impact of obesity on inflammatory stress and morbidity.

机译：住院肥胖症的真正代价：肥胖症对炎性应激和发病率的影响。

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摘要

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.
机译：本综述的目的是概述感染和损伤期间促炎性细胞因子产生的代谢作用。强调促炎细胞因子产生和炎性应激对患者发病率和死亡率的不利影响;以确定遗传和肥胖对患者炎性应激的影响，并指出营养物质如何调节患者的炎性反应。最近的研究清楚地表明，脂肪组织可以主动分泌多种促炎和抗炎细胞因子。矛盾的是，尽管炎症是人体对感染，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。炎症的代谢作用由促炎细胞因子介导。代谢作用包括胰岛素不敏感性，高血脂症，肌肉蛋白损失和氧化应激。这些作用以及在传染病期间也存在，在具有隐性炎症基础的疾病中也存在。这些后期疾病包括肥胖症和2型糖尿病。衰老过程中炎症压力也会增加。在个体内，细胞因子产生的水平受细胞因子基因中的单核苷酸多态性（SNP）的影响。 SNP的组合可控制明显和隐秘炎症疾病中炎症应激的相对水平。细胞因子基因型对源自肥胖状态的炎性应激强度的影响尚不清楚。尽管在后一种情况下仍需进行研究，但证据表明，这些基因组特征会影响传染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费用。抗氧化剂和 n -3 PUFA会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。对营养物-基因相互作用的这一方面以及影响疾病过程中炎症强度的基因组因素的更好理解将有助于更有效地靶向营养治疗。

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