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首页> 外文期刊>Research communications in molecular pathology and pharmacology >Insulin resistance and impaired endothelium-dependent renal vasodilatation in fructose-fed hypertensive rats.
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Insulin resistance and impaired endothelium-dependent renal vasodilatation in fructose-fed hypertensive rats.

机译：果糖喂养的高血压大鼠的胰岛素抵抗和内皮依赖性肾血管舒张受损。

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We investigated the contribution made by hyperinsulinemia and endothelial dysfunction to the hypertension of rats that had received 10% fructose in their drinking water for 12 weeks. As control animals with endothelial dysfunction, we used streptozotocin-induced diabetic rats. Measurements were made at 12 weeks after the start of fructose feeding or a single streptozotocin injection. Systolic blood pressure was greater in fructose-fed rats than in either streptozotocin-diabetic rats or age-matched controls. By comparison with the age-matched controls, the plasma levels of glucose, triglyceride, high density lipoprotein cholesterol, low density lipoprotein cholesterol and free fatty acids were all significantly raised in both fructose-fed rats and streptozotocin-diabetic rats. The plasma insulin was significantly raised in fructose-fed rats, whereas it was significantly lowered in streptozotocin-diabetic rats. The vasodilatation induced in the perfused kidney by acetylcholine was weaker in both fructose-fed rats and streptozotocin-diabetic rats than in the age-matched controls and these weakened responses were further attenuated by indomethacin. Acetylcholine increased the nitrite and nitrate (NO2- and NO3-) levels in the renal perfusate in age-matched controls. This effect was much weaker in the two experimental groups. These results suggest that endothelial dysfunction in fructose-fed rats and streptozotocin-diabetic rats may be due to a decreased synthesis of nitric oxide at least in the perfused kidney. It is further suggested that hyperinsulinemia is more important than endothelial dysfunction as a cause of hypertension in fructose-fed rats.
机译：我们调查了高胰岛素血症和内皮功能障碍对在饮用水中摄入10％果糖的大鼠持续12周的高血压的影响。作为具有内皮功能障碍的对照动物，我们使用链脲佐菌素诱导的糖尿病大鼠。在开始喂果糖或单次链脲佐菌素注射后第12周进行测量。用果糖喂养的大鼠的收缩压要比链脲佐菌素-糖尿病的糖尿病大鼠或年龄匹配的对照组的高。与年龄匹配的对照组相比，在果糖喂养的大鼠和链脲佐菌素-糖尿病大鼠中，血浆葡萄糖，甘油三酸酯，高密度脂蛋白胆固醇，低密度脂蛋白胆固醇和游离脂肪酸的含量均显着升高。在果糖喂养的大鼠中血浆胰岛素显着升高，而在链脲佐菌素-糖尿病大鼠中血浆胰岛素显着降低。在果糖喂养的大鼠和链脲佐菌素糖尿病的大鼠中，乙酰胆碱在灌注肾脏中诱导的血管舒张作用均弱于年龄匹配的对照组，并且吲哚美辛进一步减弱了这些减弱的反应。在年龄匹配的对照组中，乙酰胆碱会增加肾灌注液中亚硝酸盐和硝酸盐（NO2-和NO3-）的水平。在两个实验组中，这种作用要弱得多。这些结果表明，果糖喂养的大鼠和链脲佐菌素-糖尿病大鼠中的内皮功能障碍可能是由于至少在灌注肾脏中一氧化氮的合成减少。进一步提示，高果糖血症比果糖功能障碍更为重要，因为果糖喂养的大鼠会引起高血压。

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