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首页> 外文期刊>Kidney Research and Clinical Practice >Plasma leptin concentrations are greater in type II diabetic patients and stimulate monocyte chemotactic peptide-1 synthesis via the mitogen-activated protein kinase/extracellular signal-regulated kinase pathway
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Plasma leptin concentrations are greater in type II diabetic patients and stimulate monocyte chemotactic peptide-1 synthesis via the mitogen-activated protein kinase/extracellular signal-regulated kinase pathway

机译：II型糖尿病患者的血浆瘦素浓度更高，并通过促分裂原激活的蛋白激酶/细胞外信号调节激酶途径刺激单核细胞趋化肽-1的合成

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Background: Leptin is an adipokine that is recently reported to be a biomarker of systemic inflammation. Although atherosclerosis causes cardiovascular diseases, it is not clear whether leptin contributes to the acceleration of this process. In this study, we investigated whether alterations of plasma leptin levels were related to diabetic nephropathy and systemic inflammation. In addition, we examined the physiologic action of leptin in cultured vascular smooth muscle cells (VSMCs). Methods: A total of 126 type 2 diabetic participants and 37 healthy controls were studied. The diabetic participants were divided into three groups according to stage of nephropathy. We investigated whether leptin induced monocyte chemotactic peptide-1 (MCP-1) synthesis through the mitogen-activated protein kinase (MAPK) pathway using cultured VSMCs. Results: Plasma leptin concentrations were significantly higher in the diabetic group than in the controls. Plasma leptin levels were positively correlated with body mass index, fasting and postprandial blood glucose, hemoglobin A1c, total cholesterol, urinary albumin excretion, high-sensitivity C-reactive protein (hsCRP), and MCP-1 plasma levels, and negatively correlated with creatinine clearance values. In cultured VSMCs, leptin increased MCP-1 production in a dose-dependent manner, and this stimulating effect of leptin on MCP-1 expression was reversed by the MAPK (MEK) inhibitor PD98059. In addition, leptin stimulated the phosphorylation of MEK, extracellular signal-regulated kinase, and E26-like transcription factor, which are components of the MAPK pathway. Conclusions: Overall, these findings suggest that activation of leptin synthesis may promote MCP-1 activation in a diabetic environment via the MAPK pathway in VSMCs and that it possibly contributes to the acceleration of atherosclerosis.
机译：背景：瘦素是一种脂肪因子，最近被报道为全身性炎症的生物标志物。尽管动脉粥样硬化会导致心血管疾病，但尚不清楚瘦素是否有助于加速这一过程。在这项研究中，我们调查了血浆瘦素水平的变化是否与糖尿病肾病和全身性炎症有关。此外，我们检查了瘦素在培养的血管平滑肌细胞（VSMC）中的生理作用。方法：共126名2型糖尿病患者和37名健康对照者进行了研究。糖尿病参与者根据肾病的阶段分为三组。我们调查了瘦素是否通过使用培养的VSMC通过有丝分裂原激活的蛋白激酶（MAPK）途径诱导单核细胞趋化肽1（MCP-1）合成。结果：糖尿病组血浆瘦素浓度显着高于对照组。血浆瘦素水平与体重指数，禁食和餐后血糖，血红蛋白A1c，总胆固醇，尿白蛋白排泄，高敏C反应蛋白（hsCRP）和MCP-1血浆呈正相关，与肌酐负相关间隙值。在培养的VSMC中，瘦素以剂量依赖的方式增加MCP-1的产生，而瘦素对MCP-1表达的这种刺激作用被MAPK（MEK）抑制剂PD98059逆转。另外，瘦素刺激了MEK，细胞外信号调节激酶和E26样转录因子的磷酸化，它们是MAPK途径的组成部分。结论：总的来说，这些发现表明瘦素合成的激活可能通过VSMC中的MAPK途径在糖尿病环境中促进MCP-1激活，并且可能有助于动脉粥样硬化的加速。

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