Effects of 90-day hypolipidemic treatment on insulin resistance, adipokines and proinflammatory cytokines in patients with mixed hyperlipidemia and impaired fasting glucose
Effects of 90-day hypolipidemic treatment on insulin resistance, adipokines and proinflammatory cytokines in patients with mixed hyperlipidemia and impaired fasting glucose
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DOI：
10.5414/cp201735
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发表时间：
2012-11-01
影响因子：
0.8
通讯作者：
Okopien, Boguslaw
中科院分区：
文献类型：
--
作者：
Buldak, Lukasz;Dulawa-Buldak, Anna;Okopien, Boguslaw
目的：最近出现了与他汀类药物治疗相关的胰岛素敏感性恶化的担忧。因此，本研究的目的是评估和比较非诺贝特和阿托伐他汀联合治疗90天对空腹血糖（IFG）和混合性高脂血症患者空腹血糖、胰岛素抵抗指数、脂肪因子（瘦素、抵抗素、脂联素）和促炎细胞因子（tnf - α、IL-6）水平的影响。材料和方法：67例患者随机分为4个治疗组：阿托伐他汀单药治疗、非诺贝特单药治疗、非诺贝特和阿托伐他汀联合治疗或改变治疗性生活方式。试验期为90 d。所有参与者都接受了有关适当饮食和体育活动的咨询。结果：与对照组相比，糖尿病前期患者血浆瘦素、rcsistin、tnf - α和IL-6水平升高，血浆脂联素水平降低。所有的治疗干预都导致了血脂的显著改变。非诺贝特治疗后胰岛素抵抗指数（HOMA-IR）降低。阿托伐他汀对胰岛素抵抗的影响与单独改变治疗性生活方式相当。用降血脂药物治疗导致脂联素水平升高，瘦素和抵抗素水平降低。同时观察到联合治疗对血浆IL-6水平的累加效应。结论：非诺贝特治疗可改善胰岛素敏感性。阿托伐他汀未引起胰岛素敏感性的恶化。降血脂治疗导致促炎细胞因子网络和脂肪因子水平的显著变化。在研究结束时，测量的参数与健康受试者的参数几乎相似。
Objective: Concerns regarding worsening insulin sensitivity associated with statin treatment have recently emerged. Therefore the aim of this study was to assess and compare the effects of 90-day monotherapies with fenofibrate and atorvastatin, as well as combined therapy, on fasting plasma glucose, insulin resistance index, adipokines (leptin, resistin, adiponectin) and levels of proinflammatory cytokines (TNF-alpha, IL-6) in patients with impaired fasting glucose (IFG) and mixed hyperlipidemia. Materials and methods: 67 patients were randomly assigned to four treatment arms: monotherapy with atorvastatin, monotherapy with fenofibrate, combined therapy (fenofibrate and atorvastatin) or therapeutic lifestyle change. The study lasted for 90 days. All participants received counseling regarding proper diet and physical activity. Results: Compared to the control subjects, prediabetic patients exhibited elevated plasma levels of leptin, rcsistin, TNF-alpha and IL-6, and a lower plasma level of adiponectin. All therapeutic interventions resulted in significant alterations in the lipid profile. Insulin resistance index (HOMA-IR) was reduced after treatment with fenofibrate. The effect of atorvastatin on insulin resistance was comparable to therapeutic lifestyle change alone. Therapy with hypolipidemic drugs caused increases in adiponectin levels and decreases in leptin and resistin. An additive effect of the combined treatment on plasma IL-6 level was also observed. Conclusions: Fenofibrate-based treatment was associated with improved insulin sensitivity. Atorvastatin did not cause a deterioration in insulin sensitivity. Hypolipidemic therapies resulted in significant changes in the proinflammatory cytokine network as well as in adipokine levels. At the end of the study the measured parameters nearly resembled those of the healthy subjects.