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Resistin, an adipokine, may affect the improvement of insulin sensitivity in the metabolic syndrome patient treated with metformin

机译:抵抗素(一种脂肪因子)可能会影响二甲双胍治疗的代谢综合征患者的胰岛素敏感性改善

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摘要

The metabolic syndrome (MS) is a cluster of metabolic disorders arising from insulin resistance, characterized by the presence of central obesity, impaired fasting glucose level, dyslipidemia and hypertension. As the first-line medication, metformin is commonly used for MS to reduce insulin resistance. Comparing with rosiglitazone, metformin does not increase cardiovascular mortality risk in patients with MS. However, metformin is not good enough in improving insulin sensitivity. Its molecular mechanism is still not clear. Recent studies have demonstrated that resistin, an adipokine, could induce IR by both AMPK-dependent and AMPK-independent pathways. Though there were conflicting findings of resistin in metabolic syndrome or type 2 diabetes mellitus in different studies, resistin was significant decreased in the rosiglitazone treated patients than in the metformin-treated patients in most of studies. Here, we hypothesized that resistin, an adipokine, may affect the improvement of insulin sensitivity in the metabolic syndrome patient treated with metformin. This hypothesis could explain why rosiglitazone is superior to metformin in enhancement of insulin sensitivity.
机译:代谢综合症(MS)是由胰岛素抵抗引起的一组代谢紊乱,其特征为存在中枢​​肥胖,空腹血糖水平受损,血脂异常和高血压。作为一线药物,二甲双胍通常用于MS以降低胰岛素抵抗。与罗格列酮相比,二甲双胍不会增加MS患者的心血管死亡风险。但是,二甲双胍不足以改善胰岛素敏感性。其分子机制仍不清楚。最近的研究表明,抵抗素(一种脂肪因子)可以通过AMPK依赖性和AMPK依赖性途径诱导IR。尽管在不同研究中在代谢综合征或2型糖尿病中抵抗素的发现存在矛盾,但在大多数研究中,罗格列酮治疗的患者抵抗素显着低于二甲双胍治疗的患者。在这里,我们假设抵抗素(一种脂肪因子)可能会影响二甲双胍治疗的代谢综合征患者的胰岛素敏感性改善。该假设可以解释为什么罗格列酮在增强胰岛素敏感性方面优于二甲双胍。

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