title: A marked deficiency in circulating and renal IGF-I peptide does not inhibit compensatory renal enlargement in uninephrectomized mice.
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.
  
  
  METHODS
  Both IGF-I deficient (ID) and normal (N) mice underwent a uninephrectomy (UNx) and sacrificed 2 or 9days 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±39ng/g) and increased in both groups after UNx, remaining low in ID mice (45±4 in ID vs 561±64ng/g in N). IGF type 1 receptor phosphorylation was unchanged.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Pediatrics, Soroka Medical Center, Ben Gurion University of the Negev, Beer Sheva, Israel. ldaniel@bgu.ac.il
authors.forename: Daniel
authors.initials: D
authors.lastname: Landau
authors.forename: Jaclyn
authors.initials: J
authors.lastname: Biada
authors.forename: Yu
authors.initials: Y
authors.lastname: Chen
authors.forename: Sumita
authors.initials: S
authors.lastname: Sood
authors.forename: Shoshanah
authors.initials: S
authors.lastname: Yakar
authors.forename: Derek
authors.initials: D
authors.lastname: Leroith
authors.forename: Yael
authors.initials: Y
authors.lastname: Segev
authors.forename: Ralph
authors.initials: R
authors.lastname: Rabkin
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D015153:Blotting, Western; D007334:Insulin-Like Growth Factor I / Q000172:deficiency* / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D051379:Mice; D009392:Nephrectomy; D009929:Organ Size; D016133:Polymerase Chain Reaction
chemical_list: D007334:Insulin-Like Growth Factor I