The somatomedin hypothesis: 2001

D. Le Roith, C. Bondy, S. Yakar, J. L. Liu, A. Butler

Research output: Contribution to journalReview article


Since the original somatomedin hypothesis was conceived, a number of important discoveries have allowed investigators to modify the concept. Originally somatic growth was thought to be controlled by pituitary GH and mediated by circulating insulin-like growth factor-I (IGF-I, somatomedin C) expressed exclusively by the liver. With the discovery that IGF-I is produced by most, if not all, tissues, the role of autocrine/paracrine IGF-I vs. the circulating form has been hotly debated. Recent experiments using transgenic and gene-deletion technologies have attempted to answer these questions. In the liver-specific igf-1 gene-deleted mouse model, postnatal growth and development are normal despite the marked reduction in circulating IGF-I and IGF-binding protein levels; free IGF-I levels are normal. Thus, the normal postnatal growth and development in these animals may be due to normal free IGF-I levels (from as yet unidentified sources), although the role of autocrine/paracrine IGF-I has yet to be determined.

Original languageEnglish (US)
Pages (from-to)53-74
Number of pages22
JournalEndocrine Reviews
Issue number1
StatePublished - Jan 1 2001


ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Le Roith, D., Bondy, C., Yakar, S., Liu, J. L., & Butler, A. (2001). The somatomedin hypothesis: 2001. Endocrine Reviews, 22(1), 53-74.