Acarbose, an α-glucosidase inhibitor, improves endothelial dysfunction in Goto-Kakizaki rats exhibiting repetitive blood glucose fluctuation
Acarbose, an α-glucosidase inhibitor, improves endothelial dysfunction in Goto-Kakizaki rats exhibiting repetitive blood glucose fluctuation
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DOI：
10.1016/j.bbrc.2006.04.090
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发表时间：
2006-06-30
影响因子：
3.1
通讯作者：
Watada, Hirotaka
中科院分区：
文献类型：
--
作者：
Azuma, Kosuke;Toyofuku, Yukiko;Watada, Hirotaka
几项流行病学研究表明，餐后高血糖的受试者患心血管疾病的风险增加。然而，餐后高血糖及其治疗对内皮功能的影响尚不清楚。在这项研究中，Goto-Kakizaki （GK）大鼠是一种非肥胖的2型糖尿病模型，每天喂食两次作为重复餐后血糖峰值的模型。我们研究了阿卡波糖（一种α -葡萄糖苷酶抑制剂）对这些大鼠内皮功能的影响。给药12周后，阿卡波糖显著改善GK大鼠餐后高血糖、餐后胰岛素水平、总胆固醇、甘油三酯和游离脂肪酸水平。此外，阿卡波糖有效地减少了粘附在主动脉内皮层上的单核细胞数量，改善了乙酰胆碱依赖性血管舒张，减少了主动脉内膜增厚。虽然人们普遍认为重复性餐后高血糖与心血管疾病的发病有关，但我们的数据表明，阿卡波糖治疗有效地改善了内皮功能障碍，减少了内膜增厚，从而进一步支持了阿卡波糖对心血管疾病发病的保护作用。(c) 2006爱思唯尔公司版权所有。
Several epidemiological studies have revealed that subjects with postprandial hyperglycemia are at increased risk of cardiovascular disease. However, the impact of postprandial hyperglycemia and its treatment on endothelial function has not been clarified yet. In this study, Goto-Kakizaki (GK) rats, a non-obese type 2 diabetes model, fed twice daily were used as a model of repetitive postprandial glucose spikes. We investigated the endothelial function in these rats treated or untreated with acarbose, an alpha-glucosidase inhibitor. Administration of acarbose for 12 weeks markedly improved postprandial hyperglycemia, postprandial insulin level, total cholesterol, triglyceride, and free fatty acid level in GK rats. Furthermore, acarbose efficiently reduced the number of monocytes adherent to aortic endothelial layer, improved acetylcholine-dependent vasodilatation, and reduced intimal thickening of the aorta. While it is generally regarded that repetitive postprandial hyperglycemia is associated with the onset of cardiovascular diseases, our data demonstrated that acarbose treatment efficiently ameliorated endothelial dysfunction and reduced intimal thickening, thus adding support to the protective effect of acarbose against the onset of cardiovascular disease. (c) 2006 Elsevier Inc. All rights reserved.