Insulin resistance as a proinflammatory state: mechanisms, mediators, and therapeutic interventions.
Insulin resistance as a proinflammatory state: mechanisms, mediators, and therapeutic interventions.
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胰岛素抵抗作为一种促炎症状态：机制、介质和治疗干预。
DOI：
10.2174/1389450033490920
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发表时间：
2003
影响因子：
3.2
通讯作者：
P. Dandona
中科院分区：
文献类型：
--
作者：
R. Garg;D. Tripathy;P. Dandona
根据过去十年收集的科学证据，胰岛素抵抗已被认为是一种炎症性疾病。炎症标志物如CRP、PAI-1、IL-6在胰岛素抵抗患者中的浓度高于正常人。将炎症与胰岛素抵抗联系起来的机制正在探索中，并在这方面取得了进展。肿瘤坏死因子α已被证明与肥胖者的胰岛素抵抗有关。大量营养素的摄入也可能导致炎症，而禁食具有抗炎作用。胰岛素本身已被发现具有抗炎作用，这一作用可能在许多疾病状态下有用。主要作为胰岛素增敏剂的噻唑烷二酮，如罗格列酮，具有深刻的抗炎和潜在的抗动脉粥样硬化活性。考虑到与胰岛素抵抗的主要并发症动脉粥样硬化相关的发病率和死亡率，如果在长期治疗中持续下去，这些效应可能具有相当大的临床意义。
Insulin resistance has been recognized as an inflammatory disease based on the scientific evidence collected over the last decade. Inflammatory markers like CRP, PAI-1, IL-6 are present in higher concentrations in insulin resistant people than in normal people. Mechanisms, linking inflammation to insulin resistance are being explored and progress has been made in this direction. TNFalpha has been shown to be responsible for insulin resistance in obese subjects. Macronutrient intake may also induce inflammation whereas fasting has anti-inflammatory effects. Insulin itself has been found to be anti-inflammatory and this action may be useful in many disease states. Thiazolidinediones, such as rosiglitazone that act primarily as insulin sensitisers, have a profound anti-inflammatory and potentially antiatherosclerotic activity. These effects may be of considerable clinical significance if sustained during long-term therapy, given the morbidity and mortality associated with atherosclerosis, the major complication of insulin resistance.