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作 者:高宇[1] 宋光耀[1] 周宇[1] 赵晓云[1] 张海林[2]
机构地区:[1]河北省人民医院河北省老年医学重点实验室,河北石家庄050051 [2]河北医科大学药理学研究室,河北石家庄050051
出 处:《基础医学与临床》2006年第3期275-279,共5页Basic and Clinical Medicine
基 金:河北省自然基金(303552)
摘 要:目的观察高糖、高饱和及高不饱和脂肪酸饮食对大鼠胰岛素抵抗(IR)和血管内皮依赖性舒张功能的影响。方法成年Wistar大鼠随机分为对照组(NC)、高糖组(HS)、高饱和脂肪酸组(HSF)和高不饱和脂肪酸组(HUF),喂养24周后,用正葡萄糖高胰岛素钳夹技术的葡萄糖输注率(GIR)评价IR;用微血管测定技术观察肾动脉累积舒张反应。结果各实验组GIR减低,以HSF组最低,TG、FFA与GIR明显负相关;各实验组大鼠离体肾动脉环对乙酰胆碱(Ach)舒张反应减弱,HSF、HUF和HS组最大舒张反应(Rmax)分别较对照组下降37.4%、32.7%和27.7%;各实验组离体肾动脉环经左旋精氨酸(L-Arg)孵育后对Ach舒张反应增强,经L-NNA、MB孵育后舒张反应减弱;大鼠离体肾动脉环对Ach内皮依赖性舒张反应与TGI、NS明显负相关,与NO、GIR明显正相关,FFA与NO明显负相关。结论高糖、高饱和脂肪酸和高不饱和脂肪酸饮食均可诱导大鼠IR并伴有血管内皮舒张功能减弱。Objective To observe the effects of high sucrose, high saturated fatty acid and high unsaturated fatty acid diets on insulin resistance and endothelium-dependent vasodilation function. Methods Adult Wistar rats were divided into normal control (NC) group, high sucrose (HS) group and high saturated fatty acid (HSF) group, high unsaturated fatty acid (HUF) groups. Insulin sensitivity was tested by hyperinsulinemic-euglucemic clamp after 24 weeks. Acetylcholine-induced (or sodium nitroprusside-induced) relaxation of preconstricted isolated renal arteries was measured by Mulvany myograph. Results GIR was obviously lower in experimental groups than that in NC group. GIR was negatively correlated with triglyceride (TG), free fatty acid (FFA). Acetylcholine-induced relaxation was markedly decreased in all experimental groups compared with that in NC group and the maximal response was decreased 37.4% in HSF group, 32.7% in HUF group,27.7% in HS group. Acetylcholine-induced relaxation was enhanced by incubation with L-Arg and decreased incubated with L-NNA, MB in all experimental groups. Vasodilation response was negatively correlated with TG, INS and well positively correlated with NO, GIR. There was significantly negative correlation between FFA andNO. Conclusions: The rats fed high sucrose, high saturated fatty acid and high unsaturated fatty acid diets developed insulin resistance with reduced endothelium-dependent vasodilation function.
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