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Changes in adipose-derived inflammatory cytokines and chemokines after successful lifestyle intervention in obese children.

机译:成功的生活方式干预肥胖儿童后,脂肪来源的炎性细胞因子和趋化因子的变化。

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Obesity has been associated with low-grade chronic systemic inflammation, potentially leading to insulin resistance. This study was designed to examine relationships between cardiovascular risk factors, insulin resistance, and simultaneously measured inflammatory parameters in obese children. We examined serum inflammatory parameters in 115 obese children and 30 normal-weight controls; 62 obese children were followed longitudinally in a 1-year obesity intervention study. Serum concentrations of adipose tissue hormones adiponectin and resistin as well as adipocytokines were assessed. Cross-sectional analysis showed significant correlations between standard deviation score body mass index and resistin (P = .0004) as well as monocyte chemoattractant protein-1 (MCP-1, P = .04). Increased homeostasis model assessment of insulin resistance index greater than 95th percentile was present in 32% of obese patients, correlating with adiponectin (r = -0.40, P = .0007). Significant correlations were found between adiponectin and several mediators of inflammation (interleukins [ILs] IL-1beta, IL-6, and IL-8 and tumor necrosis factor-alpha). In longitudinal analysis, substantial weight loss (change standard deviation score body mass index >0.5) observed after intervention in 29 children was associated with a significant decrease in blood pressure, homeostasis model assessment of insulin resistance index, and serum concentrations of insulin and IL-1beta, IL-8, and MCP-1, but increase of adiponectin (all Ps < .05). In 33 children without substantial weight loss, resistin and MCP-1 levels increased after 1 year. Changes in IL-1beta correlated positively with changes of weight status, interferon-gamma, IL-6, IL-8, and tumor necrosis factor-alpha (all Ps < .01). Our study demonstrates significant correlations between different metabolic risk factors at baseline and after changes of weight status and that weight loss in obese children reduces low-grade inflammation, insulin resistance, and blood pressure.
机译:肥胖与低度的慢性全身性炎症有关,可能导致胰岛素抵抗。这项研究旨在检查肥胖儿童的心血管危险因素,胰岛素抵抗和同时测量的炎症参数之间的关系。我们检查了115名肥胖儿童和30名正常体重对照组的血清炎症参数;在一项为期1年的肥胖症干预研究中,对62名肥胖儿童进行了纵向随访。评估了血清脂肪组织激素脂联素和抵抗素以及脂肪细胞因子的浓度。横断面分析显示标准偏差评分体重指数与抵抗素(P = .0004)以及单核细胞趋化蛋白1(MCP-1,P = .04)之间具有显着相关性。在32%的肥胖患者中,胰岛素抵抗指数大于95%的动态平衡模型评估与脂联素相关(r = -0.40,P = .0007)。脂联素与炎症的几种介质(白介素[ILs] IL-1beta,IL-6和IL-8和肿瘤坏死因子-α)之间存在显着相关性。在纵向分析中,对29名儿童进行干预后观察到体重大量减轻(标准偏差评分体重指数> 0.5),这与血压,胰岛素抵抗指数的稳态模型评估以及血清胰岛素和IL- 1beta,IL-8和MCP-1,但脂联素增加(所有Ps <.05)。在33例体重未显着减轻的儿童中,一年后抵抗素和MCP-1水平升高。 IL-1beta的变化与体重状况,干扰素-γ,IL-6,IL-8和肿瘤坏死因子-α的变化呈正相关(所有Ps <0.01)。我们的研究表明,基线和体重状况改变后,不同代谢风险因素之间存在显着相关性,肥胖儿童的体重减轻可减轻低度炎症,胰岛素抵抗和血压。

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