TY - JOUR
T1 - IGF signaling defects as causes of growth failure and IUGR
AU - Klammt, Jürgen
AU - Pfäffle, Roland
AU - Werner, Haim
AU - Kiess, Wieland
N1 - Funding Information:
W.K. has received lecture fees and unrestricted research grant support from Novo Nordisk, Pfizer, Serono and SHS Nutrition. R.P. has received lecture fees from Eli Lilly Int., Pfizer Endocrine Care, Novo Nordisk, Ferring, Serono, Biopartners and Genentech. R.P. has also received grant support from Eli Lilly, Pfizer and Ferring. J.K. and H.W. have nothing to disclose.
Funding Information:
We thank Antje Korner and Antje Garten for critically reading the manuscript. Figure 1 was compiled using Biocarta's Pathway Templates (see: www.biocarta.com ). This work was supported in part by grants from the Interdisziplinäres Zentrum für Klinische Forschung (IZKF) Leipzig, the Deutsche Forschungsgemeinschaft (Pf225/3–1) and the PIONEER program of the European Commission.
PY - 2008/8
Y1 - 2008/8
N2 - A substantial portion of children born small for gestational age (SGA) fail to catch up height, despite normal or even elevated insulin-like growth factor (IGF1) serum levels. In most cases, the etiology of the apparent IGF1 resistance is regarded as idiopathic. However, the recent identification of human IGF1 and IGF1 receptor (IGF1R) mutations, as well as information obtained from transgenic animals, points to a strong genetic component being of pivotal importance in the development of growth retardation. These findings direct attention to molecules downstream of the IGF1R, which have both growth-promoting and, to a lesser extent, metabolic functions. Therefore, defects in these molecules are likely to participate in the etiology of human SGA.
AB - A substantial portion of children born small for gestational age (SGA) fail to catch up height, despite normal or even elevated insulin-like growth factor (IGF1) serum levels. In most cases, the etiology of the apparent IGF1 resistance is regarded as idiopathic. However, the recent identification of human IGF1 and IGF1 receptor (IGF1R) mutations, as well as information obtained from transgenic animals, points to a strong genetic component being of pivotal importance in the development of growth retardation. These findings direct attention to molecules downstream of the IGF1R, which have both growth-promoting and, to a lesser extent, metabolic functions. Therefore, defects in these molecules are likely to participate in the etiology of human SGA.
UR - http://www.scopus.com/inward/record.url?scp=47249134315&partnerID=8YFLogxK
U2 - 10.1016/j.tem.2008.03.003
DO - 10.1016/j.tem.2008.03.003
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AN - SCOPUS:47249134315
VL - 19
SP - 197
EP - 205
JO - Trends in Endocrinology and Metabolism
JF - Trends in Endocrinology and Metabolism
SN - 1043-2760
IS - 6
ER -
