Free insulin-like growth factor-1 and unilateral complete ureteral obstruction in the rat

Citation
Ta. Serel et al., Free insulin-like growth factor-1 and unilateral complete ureteral obstruction in the rat, UROLOGY, 56(5), 2000, pp. 863-866
Citations number
21
Categorie Soggetti
Urology & Nephrology
Journal title
UROLOGY
ISSN journal
00904295 → ACNP
Volume
56
Issue
5
Year of publication
2000
Pages
863 - 866
Database
ISI
SICI code
0090-4295(200011)56:5<863:FIGFAU>2.0.ZU;2-F
Abstract
Objectives. To determine the effect of unilateral ureteral obstruction on r enal free insulin-like growth factor-1 (IGF-1) content in the kidneys and t he possible role of free IGF-I in compensatory growth in the nonobstructed kidney in an experimental model. Methods. The content of free IGF-1 and total protein in the obstructed and nonobstructed kidneys were measured 7 days after unilateral ureteral obstru ction. The weights of the kidneys were also determined. The results were co mpared with those of the sham-operated animals. Results. The mean renal free IGF-1 level of the obstructed kidneys was sign ificantly lower than the mean renal free IGF-1 level of the sham-operated k idneys (P = 0.03), and the mean renal free IGF-1 level of the nonobstructed kidneys was significantly higher than the mean renal free IGF-1 level of t he sham-operated kidneys (P <0.0001). The serum free IGF-1 levels in the tw o groups were not different. The mean weight of the obstructed and nonobstr ucted kidneys was significantly higher than those of the sham-operated kidn eys (1.49 +/- 0.09 and 1.03 +/- 0.03 versus 0.88 +/- 0.02 g, P <0.0001 and P = 0.006, respectively). The obstructed kidneys had significantly lower me an protein content than the nonobstructed kidneys and had significantly hig her mean protein content than the sham-operated kidneys (P <0.0001 and P = 0.0004, respectively). Conclusions. Our results reveal that compensatory renal growth is driven by a rise in the free IGF-I concentration after unilateral ureteral obstructi on. UROLOGY 56: 863-866, 2000. (C) 2000, Elsevier Science Inc.