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首页> 外文期刊>American Journal of Physiology >PPARalpha activation elevates blood pressure and does not correct glucocorticoid-induced insulin resistance in humans.
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PPARalpha activation elevates blood pressure and does not correct glucocorticoid-induced insulin resistance in humans.

机译：PPARalpha激活会升高血压，并且不能纠正糖皮质激素诱导的人体胰岛素抵抗。

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摘要

Fibrates, activators of the nuclear receptor PPARalpha, improve dyslipidemia, but their effects on insulin resistance and vascular disease are unresolved. To test the hypothesis that PPARalpha activation improves insulin resistance and vascular function, we determined the effects of fenofibrate in healthy adults with insulin resistance induced by short-term glucocorticoid administration. Eighteen normal-weight subjects were studied in four stages: at baseline, after 21 days of fenofibrate (160 mg/day) alone, after 3 days of dexamethasone (8 mg/day) added to fenofibrate, and after 3 days of dexamethasone added to placebo (dexamethasone alone). Dexamethasone alone caused hyperinsulinemia, increased glucose, decreased glucose disposal, and reduced insulin-induced suppression of hepatic glucose production as determined by hyperinsulinemic euglycemic clamp and increased systolic blood pressure as determined by ambulatory monitoring, features associated with an insulin-resistant state. Fenofibrate improved fasting LDL and total cholesterol in the setting of dexamethasone treatment but had no significant effect on levels of insulin or glucose, insulin-stimulated glucose disposal, or insulin suppression of glucose production during clamps, or ambulatory monitored blood pressure. In the absence of dexamethasone, fenofibrate lowered fasting triglycerides and cholesterol but unexpectedly increased systolic blood pressure by ambulatory monitoring. These data suggest that PPARalpha activation in humans does not correct insulin resistance induced by glucocorticoids and may adversely affect blood pressure.
机译：纤维蛋白是核受体PPARα的激活剂，可改善血脂异常，但它们对胰岛素抵抗和血管疾病的作用尚未解决。为了检验PPARalpha激活可改善胰岛素抵抗和血管功能的假设，我们确定了非诺贝特在健康成年人中的短期糖皮质激素诱导胰岛素抵抗的作用。对18名体重正常的受试者进行了四个阶段的研究：在基线，单独服用非诺贝特21天（160毫克/天），在非诺贝特中加入3天地塞米松（8毫克/天）和添加地塞米松3天后安慰剂（单独使用地塞米松）。单用地塞米松可引起高胰岛素血症，葡萄糖增加，葡萄糖减少处置，胰岛素诱导的对肝葡萄糖生成的抑制作用减弱（由高胰岛素正常血糖钳制确定）和通过动态监测确定的收缩压升高（与胰岛素抵抗状态相关的特征）。非诺贝特在地塞米松治疗中改善了空腹低密度脂蛋白和总胆固醇，但对钳制过程中的胰岛素或葡萄糖水平，胰岛素刺激的葡萄糖处置或胰岛素抑制葡萄糖生成或动态监测血压没有显着影响。在没有地塞米松的情况下，非诺贝特通过动态监测降低了空腹甘油三酯和胆固醇，但出乎意料地增加了收缩压。这些数据表明，人体内的PPARalpha激活不能纠正糖皮质激素诱导的胰岛素抵抗，并且可能会对血压产生不利影响。

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