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Adipocytokines in metabolically healthy obesity

机译:代谢健康型肥胖中的脂肪细胞因子

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The aim of the investigation was to study the relationship among adipokines, markers of subclinical inflammation and endothelial dysfunction in patients with metabolic healthy obesity (MHO). The study included 50 persons aged 25-50 years with obesity in the absence of metabolic disorders (International Diabetes Federation criteria, 2005, marked as MHO), the control group consisted of 50 healthy respondents without obesity. We studied clinical and biochemical parameters, insulin resistance index (HOMA-IR), levels of leptin, soluble leptin receptors (sLR), resistin, adiponectin, C-reactive protein (CRP-hs), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF), endothelin-1 (ET-1), von Willebrand factor, free leptin index was calculated in a formula (FLI = leptin × 100 / sLR). In MHO patients, independently of HOMA-IR index, there was an increase in leptin, FLI, resistin, VEGF, and IL-6 parameters. The concentration of CRP-hs and TNF-α in MHO group with HOMA-IR ≥2.7 was increased. Systolic blood pressure correlated with leptin level (r=0.43, P0.05), FLI (r=0.54; P=0.01), TNF-α (r=0.44; P0.05) and IL-6 (r=0.33; P0.05); diastolic blood pressure - with leptin level (r=0.35, P0.05). Links between high density lipoproteins and leptin (r=–0.55 and r=–0.60; P0.01), resistin (r=0.32; P0.05 and r=0.60; P0.01) and VEGF (r=–0.70, P0.01) were established. The VEGF level correlated with HOMA-IR (r=0.62; P0.01), leptin (r=0.29; P0.05), FLI (r=0.50; P0.05), resistin (r=0.70; P0.01), IL-6 (r=0.74, P0.01) and ET-1 (r=0.29; P0.05). Obese patients without metabolic disorders, having normotension and normal insulin sensitivity, are less influenced to adverse cardiovascular risks due to less expressed hormonal and inflammatory activation of adipose tissue and, as a result, less pronounced endothelial dysfunction. While insulin resistance develops, cardiovascular risk increases due to activation of subclinical inflammation, angiogenic endothelial dysfunction and leptin resistance.
机译:该研究的目的是研究代谢性健康肥胖(MHO)患者的脂肪因子,亚临床炎症标志物和内皮功能障碍之间的关系。该研究纳入了50名年龄在25至50岁之间,没有代谢障碍的肥胖患者(国际糖尿病联盟标准,2005年,标记为MHO),对照组由50名健康的无肥胖者组成。我们研究了临床和生化参数,胰岛素抵抗指数(HOMA-IR),瘦素水平,可溶性瘦素受体(sLR),抵抗素,脂联素,C反应蛋白(CRP-hs),肿瘤坏死因子-α(TNF-α ),白细胞介素6(IL-6),血管内皮生长因子(VEGF),内皮素1(ET-1),血管性血友病因子,游离瘦素指数的计算公式为(FLI =瘦素×100 / sLR)。在MHO患者中,与HOMA-IR指数无关,瘦素,FLI,抵抗素,VEGF和IL-6参数增加。 HOMA-IR≥2.7的MHO组CRP-hs和TNF-α浓度升高。收缩压与瘦素水平相关(r = 0.43,P <0.05),FLI(r = 0.54; P = 0.01),TNF-α(r = 0.44; P <0.05)和IL-6(r = 0.33; P <0.05);舒张压-瘦素水平(r = 0.35,P <0.05)。高密度脂蛋白与瘦素(r = –0.55和r = –0.60; P <0.01),抵抗素(r = 0.32; P <0.05和r = 0.60; P <0.01)和VEGF(r = –0.70,P <0.01)。 VEGF水平与HOMA-IR(r = 0.62; P <0.01),瘦素(r = 0.29; P <0.05),FLI(r = 0.50; P <0.05),抵抗素(r = 0.70; P <0.01)相关。 ,IL-6(r = 0.74,P <0.01)和ET-1(r = 0.29; P <0.05)。没有血压异常和正常胰岛素敏感性的无代谢异常的肥胖患者,由于脂肪组织的激素和炎性活化表达减少,因此内皮功能障碍的发生也较轻,因此对心血管不良风险的影响较小。在胰岛素抵抗发展的同时,由于亚临床炎症的激活,血管生成内皮功能障碍和瘦素抵抗,心血管风险增加。

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