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Research Centre for Reproductive Health, Discipline of Obstetrics and Gynaecology, School of Paediatrics and Reproductive Health, University of Adelaide, Adelaide, South Australia, Australia
Submitted 2 July 2006 ; accepted in final form 8 October 2006
Appropriate partitioning of nutrients between the mother and conceptus is a major determinant of pregnancy success, with placental transfer playing a key role. Insulin-like growth factors (IGFs) increase in the maternal circulation during early pregnancy and are predictive of fetal and placental growth. We have previously shown in the guinea pig that increasing maternal IGF abundance in early to midpregnancy enhances fetal growth and viability near term. We now show that this treatment promotes placental transport to the fetus, fetal substrate utilization, and nutrient partitioning near term. Pregnant guinea pigs were infused with IGF-I, IGF-II (both 1 mg·kg–1·day–1) or vehicle subcutaneously from days 20–38 of pregnancy (term = 69 days). Tissue uptake and placental transfer of the nonmetabolizable radio analogs [3H]methyl-D-glucose (MG) and [14C]aminoisobutyric acid (AIB) in vivo was measured on day 62. Early pregnancy exposure to elevated maternal IGF-I increased placental MG uptake by >70% (P = 0.004), whereas each IGF increased fetal plasma MG concentrations by 40–50% (P < 0.012). Both IGFs increased fetal tissue MG uptake (P < 0.048), whereas IGF-I also increased AIB uptake by visceral organs (P = 0.046). In the mother, earlier exposure to either IGF increased AIB uptake by visceral organs (P < 0.014), whereas IGF-I also enhanced uptake of AIB by muscle (P = 0.044) and MG uptake by visceral organs (P = 0.016) and muscle (P = 0.046). In conclusion, exogenous maternal IGFs in early pregnancy sustainedly increase maternal substrate utilization, placental transport of MG to the fetus, and fetal utilization of substrates near term. This was consistent with the previously observed increase in fetal growth and survival following IGF treatment.
insulin-like growth factor; fetal growth; glucose transport; system A amino acid transport
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