A marked deficiency in circulating and renal IGF-I peptide does not inhibit compensatory renal enlargement in uninephrectomized mice

作者：Landau Daniel^*; Biada Jaclyn; Chen Yu; Sood Sumita; Yakar Shoshanah; LeRoith Derek; Segev Yael; Rabkin Ralph

来源：Growth Hormone & IGF Research, 2011, 21(5): 279-284.

DOI：10.1016/j.ghir.2011.07.008

• Insulin-like growth factor I
• Mice
• Gene disruption
• Knockout
• Renal hypertrophy
• Uninephrectomy
• Models
• Animal

Objective: Increase in kidney IGF-I levels due to its increased trapping from the circulation was hypothesized to be a key mediator of compensatory renal enlargement. We tested this hypothesis using genetically engineered mice with extremely low circulating IGF-I levels.
Design: Both IGF-I deficient (ID) and normal (N) mice underwent a uninephrectomy (UNx) and sacrificed 2 or 9 days later.
Results: Initial body weight (BW) and kidney weight (KW) were significantly reduced in ID vs. N mice, while KW/BW ratios were similar. MW increased post-UNx to a comparable extent in ID and N mice (125 +/- 4 and 118 +/- 6% of pre-UNx KW, p < 0.05 vs. C). Kidney IGF-I mRNA levels were similar in the ID and N mice and did not change post-UNx. Kidney IGF-I peptide levels pre-UNx were significantly lower in ID vs. N mice (25 +/- 5 vs. 305 +/- 39 ng/g) and increased in both groups after UNx, remaining low in ID mice (45 +/- 4 in ID vs 561 +/- 64 ng/g in N). IGF type 1 receptor phosphoiylation was unchanged.
Conclusion: While a severe deficiency of circulating IGF-I impairs body growth, UNx induces a significant and proportional increase in renal mass in ID mice despite markedly decreased kidney IGF-I levels (>90% reduction) and no significant change in receptor phosphorylation.

• 出版日期2011-10