Insulin-like growth factor-i promotes growth selectively in fetal
sheep in late gestation.
Lok, Fong, Julie A. Owens, Linda Mundy, Jeffrey S. Robinson, and
Phillip C. Owens.
Department of Obstetrics and Gynaecology, University of Adelaide,
SA 5005, AUSTRALIA and CSIRO Division of Human Nutrition, Cooperative
Research Centre for Tissue Growth and Repair, PO Box 10065, Adelaide,
SA, 5000, Australia
APStracts 2:0333R, 1995.
Insulin-like growth factor-I (IGF-I) is required for normal fetal
growth and skeletal maturation in late gestation, since null
mutations of the IGF-I gene in mice reduce fetal weight and retard
ossification of bones. To determine if conversely, increased
abundance of IGF-I promotes fetal growth and skeletal maturation,
fetal sheep were infused intravascularly with recombinant human IGF-I
(n=7) (26+3 [mu]g/ hr/ kg) from 120 to 130 days gestation and
compared to controls (n=15). IGF-I infusion increased plasma IGF-I
concentrations by 140% (p=0.002) and weights of fetal liver, lungs,
heart, kidneys, spleen, pituitary, and adrenal glands by 16 to 50%
(p<0.05). Weights and/ or lengths of the fetus, placenta,
gastrointestinal tract, individual skeletal muscles, and long bones
were unchanged by IGF-I. However, IGF-I increased the percentage of
proximal epiphyses of long bones present (p<0.05) and their
cross-sectional areas by 15 to 38% (p<0.05). These results show
that IGF-I promotes growth of major fetal organs, endocrine glands
and skeletal maturation in vivo, consistent with IGF-I actively
controlling and not merely facilitating fetal growth. The variable
response of different tissues may partly reflect tissue specificity
in growth requirements for additional factors.
Received 19 June 1995; accepted in final form 18 October 1995.
APS Manuscript Number R371-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95