Roysommuti Sanya, Khongnakha Thidarat, Jirakulsomchok Dusit, Wyss J Michael
Department of Physiology, Faculty of Medicine, Khon Kaen University, Thailand.
Am J Hypertens. 2002 Sep;15(9):773-9. doi: 10.1016/s0895-7061(02)02974-6.
Diets high in carbohydrates are associated with hypertension, activation of the renin-angiotensin system, hyperinsulinemia, insulin resistance, and renal dysfunction. This study tests the hypothesis that the initial effect of a long-term high carbohydrate diet is a renin-angiotensin system dependant impairment of renal function.
Three-week-old male Sprague-Dawley rats drank water containing 5% glucose or water alone. Four weeks later, arterial pressure was continuously recorded in conscious restrained rats. Urine and blood samples were collected by catheter before, during, and after intravenous saline infusion, and fasting glucose tolerance tests were performed to estimate insulin resistance. To assess the possible role of the renin-angiotensin system, a group of glucose-fed rats was treated with oral captopril for 2 days before the renal function study.
Despite slightly and significantly lowered body weight, the treatments did not significantly alter heart and kidney weights, arterial pressure, or heart rate. Non-fasting blood sugar levels were slightly higher in the two groups of glucose-fed rats compared with the control rats (P < .05), but fasting blood sugar concentration and glucose tolerance were not significantly different among groups. The glucose-fed rats displayed significantly impaired renal diuresis and natriuresis as well as significantly elevated glomerular filtration rate and filtration fraction, but administration of captopril corrected these impairments. Effective renal blood flow and renal vascular resistance were not significantly different among groups.
These results indicate that diets high in carbohydrates impair renal function before they increase arterial pressure, and that this effect is dependent on an intact renin-angiotensin system.
高碳水化合物饮食与高血压、肾素 - 血管紧张素系统激活、高胰岛素血症、胰岛素抵抗及肾功能障碍有关。本研究检验了以下假设:长期高碳水化合物饮食的初始效应是肾素 - 血管紧张素系统依赖性的肾功能损害。
3周龄雄性Sprague - Dawley大鼠饮用含5%葡萄糖的水或仅饮用普通水。4周后,对清醒受限的大鼠连续记录动脉血压。在静脉输注生理盐水前、期间和之后,通过导管收集尿液和血液样本,并进行空腹葡萄糖耐量试验以评估胰岛素抵抗。为评估肾素 - 血管紧张素系统的可能作用,在进行肾功能研究前2天,对一组喂食葡萄糖的大鼠口服卡托普利进行治疗)。
尽管体重略有显著下降,但这些处理并未显著改变心脏和肾脏重量、动脉血压或心率。两组喂食葡萄糖的大鼠非空腹血糖水平略高于对照大鼠(P < 0.05),但各组间空腹血糖浓度和葡萄糖耐量无显著差异。喂食葡萄糖的大鼠表现出明显受损的肾利尿和钠利尿作用,以及显著升高的肾小球滤过率和滤过分数,但给予卡托普利可纠正这些损害。各组间有效肾血流量和肾血管阻力无显著差异。
这些结果表明,高碳水化合物饮食在升高动脉血压之前就会损害肾功能,且这种效应依赖于完整的肾素 - 血管紧张素系统。