It has been shown that IGF-I has an anabolic effect in the normal fetus. Ho
wever, there is evidence to suggest that there may be IGF-I resistance in t
he growth retarded fetus. Therefore, we investigated the effects of acute I
GF-I infusion to chronically catheterised fetal sheep. At 128 days gestatio
n, fetuses underwent a 4 h infusion of IGF-I (50 mu g/kg/h). Three groups o
f animals were studied. Nine normally grown fetuses were studied as control
s. Embolised animals (n=8) received microspheres into the uterine vasculatu
re, and animals with spontaneous intra-uterine growth retardation (IUGR ani
mals) (n=6) were fetuses found at post mortem to be spontaneously growth re
stricted.
The effects of IGF-I infusion on fete-placental carbohydrate and protein me
tabolism were similar in our control group to previous similar experiments.
IGF-I infusion decreased fetal blood glucose, oxygen, urea and amino-nitro
gen concentrations, and inhibited placental lactate production. The same fe
tal blood metabolite concentrations also fell during IGF-I infusion in the
embolised fetuses, but the effect on placental lactate production was not s
een. The only effect of IGF-I infusion in the spontaneous IUGR animals was
a fall in fetal blood amino-nitrogen concentrations. We conclude that fetal
IGF-I infusion does not have the same anabolic effects in the growth retar
ded fetus as the normal fetus. In addition, the effects of IGF-I were diffe
rent in the two growth retarded groups. Our data support previous evidence
that the growth retarded fetus has altered IGF-I sensitivity, and this may
vary depending on the cause, severity and duration of growth retardation.