Abstract:OBJECTIVE: To investigate the effects of malnutrition, nephrosis itself and glucocorticoid therapy on IGF-I/IGFBPs mRNA expressions in the rat liver and kidney, and serum peptides. METHODS: Twenty four male SpragueDawley (SD) rats were randomly grouped into control, pair fed, doxorubincininduced nephrotic and examethasonetreated nephrotic rats. IGF-I/IGFBPs mRNA in the rat liver and kidney, and serum peptides were measured by RT-PCR, RIA and Western ligand blot respectively. RESULTS: ①Reduced serum IGF-I was caused by malnutrition and glucocorticoid therapy rather than nephrosis itself, but IGF-IA mRNA in rat liver and kidney was increased during malnutrition, reduced during glucocorticoid therapy, and unchanged during nephrosis. ②IGFBP-2 mRNA in the rat liver and serum peptides decreased during malnutrition, and were elevated during nephrosis, but serum IGFBP-2 was not changed during glucocorticoid therapy despite its diminished gene expression in the rat liver and kidney. However, IGFBP-2 mRNA in the rat kidney was unchanged during malnutrition, and reduced during nephrosis. ③Serum IGFBP-3 decreased during malnutrition and nephrosis, and increased during glucocorticoid therapy, but reduced IGFBP-3 mRNA in the rat liver was observed during nephrosis and glucocorticoid therapy rather than malnutrition. IGFBP-3 mRNA in the rat kidney was only detectable during glucocorticoid therapy. CONCLUSIONS: The regulation of nutrition, nephrosis and glucocorticoid on IGF-I/IGFBPsd mRNA expressions in the rat liver and kidney is organspecific. The disturbance of serum IGFBPs in the nephrotic syndrome are mainly due to altered liver synthesis except that low serum IGF-I is partly caused by reduced renal synthesis. IGFBPs might regulate the action of IGF-I at different levels in the nephrotic syndrome.
