吡伐他汀治疗对日本男性空腹和餐后糖脂代谢和氧化应激的短期影响

Cholesterol Pub Date : 2013-01-01 Epub Date: 2013-12-10 DOI:10.1155/2013/314170
Hirokazu Kakuda, Junji Kobayashi, Mio Nakato, Noboru Takekoshi
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引用次数: 14

摘要

介绍。本研究的目的是阐明匹伐他汀如何影响糖脂代谢、肾功能和氧化应激。方法。10名日本男性(平均年龄33.9岁)口服匹伐他汀2mg,持续4周。在匹伐他汀治疗0和4周(每天2毫克一次)时,评估餐后葡萄糖、脂蛋白代谢和氧化应激标志物,测试餐包括总热量:460千卡、碳水化合物:56.5克(226千卡)、蛋白质:18克(72千卡)、脂质:18克(162千卡)和NaCl: 1.6克。在试验餐摄入后0、60和120分钟测量代谢参数。结果。给予匹伐他汀后,血清总胆固醇、低密度脂蛋白胆固醇、载脂蛋白B、花生四烯酸、胰岛素和尿尿酸排泄均降低,肌酐清除率(ccr)和尿酸清除率(cua)升高。餐后尿8-羟基脱氧鸟苷与空腹尿8-羟基脱氧鸟苷保持不变,而吡伐他汀治疗后餐后尿异前列腺素与空腹尿异前列腺素降低。接下来,我们比较了服用匹伐他汀前后的餐后葡萄糖和脂质代谢。甘油三酯(P < 0.05)和残余样颗粒胆固醇(P < 0.01)的曲线下增量面积显著减少,而载脂蛋白E (apoE)、葡萄糖、胰岛素和高敏c反应蛋白的曲线下增量面积保持不变。结论。匹伐他汀改善餐后氧化应激和高脂血症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Short-term effect of pitavastatin treatment on glucose and lipid metabolism and oxidative stress in fasting and postprandial state using a test meal in Japanese men.

Short-term effect of pitavastatin treatment on glucose and lipid metabolism and oxidative stress in fasting and postprandial state using a test meal in Japanese men.

Short-term effect of pitavastatin treatment on glucose and lipid metabolism and oxidative stress in fasting and postprandial state using a test meal in Japanese men.

Short-term effect of pitavastatin treatment on glucose and lipid metabolism and oxidative stress in fasting and postprandial state using a test meal in Japanese men.

Introduction. The objective of this study was to clarify how pitavastatin affects glucose and lipid metabolism, renal function, and oxidative stress. Methods. Ten Japanese men (average age of 33.9 years) were orally administered 2 mg of pitavastatin for 4 weeks. Postprandial glucose, lipoprotein metabolism, and oxidative stress markers were evaluated at 0 and 4 weeks of pitavastatin treatment (2 mg once daily) with a test meal consisting of total calories: 460 kcal, carbohydrates: 56.5 g (226 kcal), protein: 18 g (72 kcal), lipids: 18 g (162 kcal), and NaCl: 1.6 g. Metabolic parameters were measured at 0, 60, and 120 minutes after test meal ingestion. Results. After administration of pitavastatin, serum total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, arachidonic acid, insulin, and adjusted urinary excretion of uric acid decreased, whereas creatinine clearance (C Cr) and uric acid clearance (C UA) increased. And postprandial versus fasting urine 8-hydroxydeoxyguanosine remained unchanged, while postprandial versus fasting isoprostane decreased after pitavastatin treatment. Next, we compared postprandial glucose and lipid metabolism after test meal ingestion before and after pitavastatin administration. Incremental areas under the curve significantly decreased for triglycerides (P < 0.05) and remnant-like particle cholesterol (P < 0.01), while those for apolipoprotein E (apoE), glucose, insulin, and high-sensitivity C-reactive protein remained unchanged. Conclusion. Pitavastatin improves postprandial oxidative stress along with hyperlipidemia.

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