The IGF-I axis in kidney and skeletal muscle of potassium deficient rats

Abstract

Potassium deficiency in the rat results in growth retardation, muscle wasting and renal hypertrophy. This study tests the thesis that K deficiency leads to tissue distinct changes in the local IGF-I system and cell sensitivity to IGF-I that favors renal enlargement on the one hand and impaired muscle growth on the other. In rats after eight days of K deficiency, compared to pair-fed control rats, food utilization and muscle and body wt gain were attenuated while the kidneys enlarged. In muscle GH receptor and IGF-I gene expression, IGF-I peptide and IGF binding protein-5 (IGFBP) levels were decreased. Together with reduced food utilization, these changes may contribute to the attenuated muscle growth. In the enlarged kidneys despite a fall in IGF-I mRNA level, IGF-I peptide concentration was increased more than twofold. This increase in IGF-I could be caused by the increase in kidney IGFBP-1 gene and protein expression and the decrease in kidney IGF-I degrading activity noted in K deficiency. Treatment with IGF-I failed to induce body or muscle growth, but induced a further increase in kidney size and enlargement of the spleen. Thus, in K deficiency the spontaneous increase in IGF-I levels in the kidney that is IGF-I sensitive may well be a cause of the renal hypertrophy.