IGF, TYPE-I IGF RECEPTOR AND IGF-BINDING PROTEIN MESSENGER-RNA EXPRESSION IN KIDNEY AND LIVER OF POTASSIUM-DEPLETED AND NORMAL RATS INFUSEDWITH IGF-I

Dietary potassium (Ii) depletion is known to reduce body weight gain a nd organ growth, except for kidney which increases in weight. This ren al hypertrophy is preceded by increased renal IGF-I levels. In the pre sent study, we investigated IGF-I and -II, type I IGF receptor and IGF -binding protein (IGFBP) mRNA expression in liver and kidney of ii-dep leted and normal rats infused with vehicle or recombinant human IGF-I. Body weight gain was almost completely arrested in Ii-depleted rats w ithout any stimulatory effect of IGF-I infusion. Both absolute and rel ative kidney weight (kidney weight/body weight) were significantly inc reased in Ii-depleted rats and this was further enhanced by IGF-I infu sion. In contrast, relative liver weight was comparable in the differe nt groups and unaffected by IGF-I infusion. IGF-I mRNA expression was significantly lower in kidney and liver of Ii-depleted animals whereas type I IGF receptor levels were unchanged. In contrast, in kidney, Ii depletion increased IGFBP-1 and -2 mRNA expression with no additional effect of IGF-I infusion. In liver of Ii-depleted animals, IGFBP-1 mR NA expression was increased whereas increased IGFBP-1 and -2 mRNA expr ession was observed when these animals were infused with IGF-I. These observations may point towards a differential mode of action of the IG FBPs. In kidney increased IGFBP-1 and -2 mRNA expression may enhance I GF-I bioavailability with subsequent kidney growth. In liver, with cle arly detectable type I IGF receptor mRNA expression, increased IGFBP l evels may protect from IGF-I-induced organ growth by decreasing IGF-I bioavailability.