Abstract:
Soy protein slows disease progression and modifies fatty acid status in kidney and liver tissues after 6 weeks of feeding in the Han:SPRD-' cy' rat model of poly ystic kidney disease. To determine whether early dietary soy protein feeding alters the progression of chronic renal disease, renal and hepatic fatty acid status, and renal ex vivo release of PGE 2, three-week-old heterozygous male Han:SPRD-'cy' rats (n = 87) were given 20% casein or soy protein based diets for 1 or 3 weeks. Immunohistochemical analysis revealed that soy feeding reduced fibrous volume after 1 week of feeding and renal cyst volume after 3 weeks of feeding in diseased animals. Fatty acid analysis revealed that soy feeding elevated kidney linoleic acid (weight %) in both normal and diseased animals at 1 week (15.81 +- 0.25% vs 12.16 +- 0.24%, P < 0.05) but not at 3 weeks. Lower renal arachidonic acid was observed at 3 weeks in diseased animals (24.32 +- 0.87% vs 27.77 +- 1.05%, P < 0.05) compared to normals, with no effect of diet observed. Similar to the kidney, hepatic linoleic acid was elevated by dietary soy protein at 1 week (17.34 +- 0.26 vs 13.82 +- 0.27%, P < 0.05) but not at 3 weeks. Hepatic arachidonic acid content was higher overall in soy fed animals when compared to casein fed animals (19.50 +- 0.34 vs 17.74 +- 0.34%, P < 0.05). Whole tissue ex vivo release of prostaglandin E2 (nmol/kidney) doubled in diseased animals from 1 to 3 weeks of feeding while normal animals remained consistent over time. Soy protein alters renal fibrous volume and renal and hepatic fatty acid composition after 1 week of dietary intervention. After only 3 weeks of feeding, soy demonstrates an overall attenuation of early renal disease progression, emphasizing the importance of early dietary intervention in this disease.
