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

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...

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Pubblicato in:Growth Horm IGF Res
Autori principali: Landau, Daniel, Biada, Jaclyn, Chen, Yu, Sood, Sumita, Yakar, Shoshanah, LeRoith, Derek, Segev, Yael, Rabkin, Ralph
Natura: Artigo
Lingua:Inglês
Pubblicazione: 2011
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Article
Accesso online:https://ncbi.nlm.nih.gov/pmc/articles/PMC5488277/
https://ncbi.nlm.nih.gov/pubmed/21862442
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.ghir.2011.07.008
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