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补充L-精氨酸可改善高蛋白饮食喂养大鼠的肾肥大。

Dietary supplementation of L-arginine ameliorates renal hypertrophy in rats fed a high-protein diet.

作者信息

Reyes A A, Klahr S

机构信息

Department of Medicine, Washington University School of Medicine at Jewish Hospital of St. Louis, Missouri 63110.

出版信息

Proc Soc Exp Biol Med. 1994 Jun;206(2):157-61. doi: 10.3181/00379727-206-43735.

DOI:10.3181/00379727-206-43735
PMID:8208740
Abstract

Ingestion of a high-protein diet or intravenous administration of amino acids is associated with an increase in glomerular filtration rate (GFR). It can also lead to renal hypertrophy, and, if sustained, may cause glomerular sclerosis. L-Arginine administration ameliorates the progression of renal disease in rats with subtotal nephrectomy and prevents the increase in GFR observed in rats with experimental diabetes. The present study examines the potential effect(s) of L-arginine administration (1%) in the drinking water on the renal hypertrophy that occurs in rats fed a high-protein diet for 1 month. Four groups of female Sprague-Dawley rats, six in each group, were studied (95 +/- 1 g). Groups 1 and 2 were fed a low-protein diet (12% casein, 0.504% L-arginine); Group 1 was given tap water, whereas Group 2 was given tap water supplemented with L-arginine. Groups 3 and 4 were fed a high-protein diet (40% casein, 1.68% L-arginine); Group 3 was given tap water, whereas Group 4 was given tap water supplemented with L-arginine. The rats had free access to food and water during the study period. The kidney weight and the kidney to body weight ratio of rats of Group 3 were significantly greater than in the other groups of rats. Renal hypertrophy was prevented in the rats of Group 4. The excretion of orotic acid in the urine, an index of L-arginine deficiency, was significantly greater in rats of Group 3 than in rats of Group 4. Thus, the renal hypertrophy that occurs in rats fed a high-protein diet was decreased in rats given L-arginine supplementation in the drinking water. This effect was associated with less excretion of orotic acid in the urine in rats given L-arginine. A relative deficiency of L-arginine may occur during high-protein feeding that may shunt nitrogen metabolism from the urea cycle to the orotic acid pathway.

摘要

摄入高蛋白饮食或静脉注射氨基酸与肾小球滤过率(GFR)增加有关。它还可导致肾脏肥大,如果持续存在,可能会引起肾小球硬化。给予L-精氨酸可改善大鼠肾次全切除术后肾病的进展,并防止实验性糖尿病大鼠出现GFR升高。本研究探讨了在饮用水中给予1%L-精氨酸对喂食高蛋白饮食1个月的大鼠发生肾脏肥大的潜在影响。研究了四组雌性Sprague-Dawley大鼠,每组6只(体重95±1g)。第1组和第2组喂食低蛋白饮食(12%酪蛋白,0.504%L-精氨酸);第1组给予自来水,而第2组给予补充L-精氨酸的自来水。第3组和第4组喂食高蛋白饮食(40%酪蛋白,1.68%L-精氨酸);第3组给予自来水,而第4组给予补充L-精氨酸的自来水。在研究期间,大鼠可自由获取食物和水。第3组大鼠的肾脏重量和肾脏与体重之比显著高于其他组大鼠。第4组大鼠的肾脏肥大得到预防。作为L-精氨酸缺乏指标的尿乳清酸排泄量,第3组大鼠显著高于第4组大鼠。因此,在饮用水中补充L-精氨酸的大鼠中,喂食高蛋白饮食的大鼠发生的肾脏肥大有所减轻。这种作用与给予L-精氨酸的大鼠尿中乳清酸排泄减少有关。在高蛋白喂养期间可能会出现L-精氨酸相对缺乏,这可能会使氮代谢从尿素循环转向乳清酸途径。

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Dietary supplementation of L-arginine ameliorates renal hypertrophy in rats fed a high-protein diet.补充L-精氨酸可改善高蛋白饮食喂养大鼠的肾肥大。
Proc Soc Exp Biol Med. 1994 Jun;206(2):157-61. doi: 10.3181/00379727-206-43735.
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Dietary supplementation with L-arginine ameliorates the progression of renal disease in rats with subtotal nephrectomy.用L-精氨酸进行膳食补充可改善大鼠肾次全切除术后肾病的进展。
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Dietary supplementation with L-arginine ameliorates glomerular hypertension in rats with subtotal nephrectomy.L-精氨酸膳食补充剂可改善大鼠肾次全切除术后的肾小球高血压。
J Am Soc Nephrol. 1994 Mar;4(9):1690-4. doi: 10.1681/ASN.V491690.
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L-arginine administration prevents glomerular hyperfiltration and decreases proteinuria in diabetic rats.给予L-精氨酸可预防糖尿病大鼠的肾小球高滤过并减少蛋白尿。
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Paradoxical increase in nitric oxide synthase activity in hypercholesterolaemic rats with impaired renal function and decreased activity of nitric oxide.肾功能受损且一氧化氮活性降低的高胆固醇血症大鼠中一氧化氮合酶活性的反常增加。
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Mechanism of compensatory renal hypertrophy.代偿性肾肥大的机制。
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Urinary metabolites characteristic of urea-cycle amino acid deficiency.尿素循环氨基酸缺乏的尿液代谢物特征。
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Nutritional and metabolic effects and significance of mild orotic aciduria during dietary supplementation with arginine or its organic salts after trauma injury in rats.大鼠创伤损伤后补充精氨酸或其有机盐期间轻度乳清酸尿症的营养和代谢影响及意义
Metabolism. 1997 Jul;46(7):785-92. doi: 10.1016/s0026-0495(97)90123-2.

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