Sánchez-Lozada Laura G, Tapia Edilia, Jiménez Adriana, Bautista Pablo, Cristóbal Magdalena, Nepomuceno Tomás, Soto Virgilia, Avila-Casado Carmen, Nakagawa Takahiko, Johnson Richard J, Herrera-Acosta Jaime, Franco Martha
Dept. of Nephrology, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1. 14080, Mexico City, Mexico.
Am J Physiol Renal Physiol. 2007 Jan;292(1):F423-9. doi: 10.1152/ajprenal.00124.2006. Epub 2006 Aug 29.
Fructose intake has been recently linked to the epidemic of metabolic syndrome and, in turn, the metabolic syndrome has been epidemiologically linked with renal progression. The renal hemodynamic effects of fructose intake are unknown, as well as the effects of different routes of administration. Metabolic syndrome was induced in rats over 8 wk by either a high-fructose diet (60%, F60, n = 7) or by adding fructose to drinking water (10%, F10, n = 7). Body weight and food and fluid intake of each rat were measured weekly during the follow-up. At baseline and at the end of wk 8, systolic blood pressure, plasma uric acid, and triglycerides were measured. At the end of week 8 glomerular hemodynamics was evaluated by micropuncture techniques. Wall thickening in outer cortical and juxtamedullary afferent arterioles was assessed by immunohistochemistry and computer image analysis. Fructose administration either in diet or drinking water induced hypertension, hyperuricemia, and hypertriglyceridemia; however, there was a progressive increment in these parameters with higher fructose intake (C<F10<F60). In addition, the F60 rats developed kidney hypertrophy, glomerular hypertension, cortical vasoconstriction, and arteriolopathy of preglomerular vessels. In conclusion, fructose-induced metabolic syndrome is associated with renal disturbances characterized by renal hypertrophy, arteriolopathy, glomerular hypertension, and cortical vasoconstriction. These changes are best observed in rats administered high doses (60% diet) of fructose.
果糖摄入近来被认为与代谢综合征的流行有关，而代谢综合征在流行病学上又与肾脏病变进展相关。果糖摄入对肾脏血流动力学的影响尚不清楚，不同给药途径的影响也不清楚。通过高果糖饮食（60%，F60，n = 7）或在饮用水中添加果糖（10%，F10，n = 7），在8周内诱导大鼠发生代谢综合征。在随访期间每周测量每只大鼠的体重、食物和液体摄入量。在基线和第8周结束时，测量收缩压、血浆尿酸和甘油三酯。在第8周结束时，通过微穿刺技术评估肾小球血流动力学。通过免疫组织化学和计算机图像分析评估皮质外层和近髓传入小动脉的壁增厚情况。饮食或饮用水中给予果糖均可诱发高血压、高尿酸血症和高甘油三酯血症；然而，随着果糖摄入量增加，这些参数呈逐渐上升趋势（对照组<F10<F60）。此外，F60组大鼠出现肾肥大、肾小球高血压、皮质血管收缩和肾小球前血管的小动脉硬化。总之，果糖诱导的代谢综合征与以肾肥大、小动脉硬化、肾小球高血压和皮质血管收缩为特征的肾脏紊乱有关。这些变化在给予高剂量（60%饮食）果糖的大鼠中最为明显。
