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

Daniel Landau, Jaclyn Biada, Yu Chen, Sumita Sood, Shoshanah Yakar, Derek LeRoith, Yael Segev, Ralph Rabkin

Research output: Contribution to journalArticlepeer-review

Abstract

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. KW 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 phosphorylation 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. This all suggests that factors other than circulating and locally produced IGF-I are responsible for compensatory renal enlargement.

Original languageEnglish (US)
Pages (from-to)279-284
Number of pages6
JournalGrowth Hormone and IGF Research
Volume21
Issue number5
DOIs
StatePublished - Oct 2011

Keywords

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

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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