The somatomedin hypothesis: 2001

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

Research output: Contribution to journalArticle

Abstract

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
Volume22
Issue number1
DOIs
StatePublished - 2001

Fingerprint

Somatomedins
Insulin-Like Growth Factor I
Growth and Development
Insulin-Like Growth Factor Binding Proteins
Liver
Gene Deletion
Research Personnel
Technology
Growth

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

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. https://doi.org/10.1210/er.22.1.53

The somatomedin hypothesis : 2001. / Le Roith, D.; Bondy, C.; Yakar, Shoshana; Liu, J. L.; Butler, A.

In: Endocrine Reviews, Vol. 22, No. 1, 2001, p. 53-74.

Research output: Contribution to journalArticle

Le Roith, D, Bondy, C, Yakar, S, Liu, JL & Butler, A 2001, 'The somatomedin hypothesis: 2001', Endocrine Reviews, vol. 22, no. 1, pp. 53-74. https://doi.org/10.1210/er.22.1.53
Le Roith, D. ; Bondy, C. ; Yakar, Shoshana ; Liu, J. L. ; Butler, A. / The somatomedin hypothesis : 2001. In: Endocrine Reviews. 2001 ; Vol. 22, No. 1. pp. 53-74.
@article{a821c237eb684726bbb406be346d93a8,
title = "The somatomedin hypothesis: 2001",
abstract = "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.",
author = "{Le Roith}, D. and C. Bondy and Shoshana Yakar and Liu, {J. L.} and A. Butler",
year = "2001",
doi = "10.1210/er.22.1.53",
language = "English (US)",
volume = "22",
pages = "53--74",
journal = "Endocrine Reviews",
issn = "0163-769X",
publisher = "The Endocrine Society",
number = "1",

}

TY - JOUR

T1 - The somatomedin hypothesis

T2 - 2001

AU - Le Roith, D.

AU - Bondy, C.

AU - Yakar, Shoshana

AU - Liu, J. L.

AU - Butler, A.

PY - 2001

Y1 - 2001

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0035115801&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035115801&partnerID=8YFLogxK

U2 - 10.1210/er.22.1.53

DO - 10.1210/er.22.1.53

M3 - Article

C2 - 11159816

AN - SCOPUS:0035115801

VL - 22

SP - 53

EP - 74

JO - Endocrine Reviews

JF - Endocrine Reviews

SN - 0163-769X

IS - 1

ER -