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首页> 外文期刊>The journal of clinical endocrinology and metabolism >Analysis of Insulin Sensitivity in Adipose Tissue of Patients with Primary Aldosteronism
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Analysis of Insulin Sensitivity in Adipose Tissue of Patients with Primary Aldosteronism

机译：原发性醛固酮增多症患者脂肪组织中胰岛素敏感性的分析

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Objective: The objective of the study was to assess the effect of high aldosterone levels on insulin sensitivity of adipose tissue in humans.Methods: Visceral adipose tissue (VAT) was obtained from patients with aldosterone-producing adenoma (APA; n=14) and, as controls, nonfunctioning adenoma (NFA; n = 14) undergoing laparoscopic adrenalectomy. Homeostasis model assessment index was higher and potassium was lower in APA than NFA ( P < 0.05). Immunohistochemistry, Western blotting, and real-time PCR were used to detect and quantify mineralocorticoid receptor (MR) expression. Transcript levels of peroxisome proliferative-activated receptor-γ, insulin receptor, glucose transporter 4, insulin receptor substrate-1 and -2, leptin, adiponectin, IL-6, monocyte chemoattractant protein-1, glucocorticoid receptor (GR)-α, 11β-hydroxysteroid dehydrogenase (HSD11B) type 1, and HSD11B2 were quantified. The effect of increasing aldosterone concentrations on 2-deoxy-[~(3)H] d -glucose uptake was tested in human sc abdominal adipocytes.Results: Expression of MR was demonstrated in VAT, with no difference between APA and NFA as to mRNA levels of MR, GRα, HSD11B1, and glucose metabolism and inflammation factors. In cultured adipocytes, basal and insulin-stimulated glucose uptake were unaffected by 1–100 nm(normal/hyperaldosteronism) and impaired only by much higher, up to 10 μm, aldosterone concentrations. The impairment was prevented by RU486 but not by eplerenone.Conclusions: Gene expression of insulin signaling/inflammatory molecules was similar in VAT of APA and NFA patients, not supporting an effect of aldosterone excess on insulin sensitivity of adipose tissues. Only at pharmacological concentrations and through GR activation, aldosterone reduced glucose uptake in adipocytes. Insulin resistance in primary aldosteronism might occur in compartments other than fat and/or depend on concurrent environmental factors.
机译：目的：研究目的是评估高醛固酮水平对人体脂肪组织胰岛素敏感性的影响。方法：内脏脂肪组织（VAT）来自产生醛固酮的腺瘤（APA; n = 14）和作为对照，行腹腔镜肾上腺切除术的无功能腺瘤（NFA; n = 14）。与NFA相比，APA中的稳态模型评估指数更高，钾更低（P <0.05）。免疫组织化学，蛋白质印迹和实时PCR用于检测和定量盐皮质激素受体（MR）的表达。过氧化物酶体增殖激活受体γ，胰岛素受体，葡萄糖转运蛋白4，胰岛素受体底物-1和-2，瘦素，脂联素，IL-6，单核细胞趋化蛋白-1，糖皮质激素受体（GR）-α，11β的转录水平定量1型-羟基类固醇脱氢酶（HSD11B）和HSD11B2。在人皮下腹部脂肪细胞中检测了醛固酮浓度升高对2-脱氧-[〜（3）H] d-葡萄糖摄取的影响。结果：在增值税中证实了MR的表达，APA和NFA在mRNA上无差异MR，GRα，HSD11B1的水平以及葡萄糖代谢和炎症因子。在培养的脂肪细胞中，基础和胰岛素刺激的葡萄糖摄取不受1–100 nm（正常/醛固酮增多症）的影响，并且仅在高得多（至多10μm）的醛固酮浓度时受到损害。结论：RU486可预防这种损伤，而依普利酮则不能。结论：APA和NFA患者的增值税中胰岛素信号/炎症分子的基因表达相似，不支持醛固酮过量对脂肪组织胰岛素敏感性的影响。仅在药理浓度和通过GR激活后，醛固酮才会降低脂肪细胞中的葡萄糖摄取。原发性醛固酮增多症中的胰岛素抵抗可能发生在脂肪以外的隔室中和/或取决于并发的环境因素。

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