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|Title:||Insulin-like growth factor-I promotes growth selectively in fetal sheep in late gestation|
|Citation:||American Journal of Physiology. Regulatory Integrative and Comparative Physiology, 1996; 270(5):R1148-R1155|
|Publisher:||American Physiological Society|
|Fong Lok, Julie A. Owens, Linda Mundy, Jeffrey S. Robinson, and Phillip C. Owens|
|Abstract:||Insulin-like growth factor I (IGF-I) is required for normal fetal growth and skeletal maturation in late gestation, because 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 micrograms. h-1.kg-1) from 120 to 130 days gestation and compared with 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 16-50% (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.|
|Keywords:||Musculoskeletal System; Fetal Blood; Fetus; Placenta; Animals; Sheep; Humans; Insulin; Insulin-Like Growth Factor I; Insulin-Like Growth Factor II; Recombinant Proteins; Embryonic and Fetal Development; Bone Development; Pregnancy; Female|
|Rights:||Copyright © 1996 the American Physiological Society|
|Appears in Collections:||Physiology publications|
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