TY - JOUR
T1 - Early treatment of the pregnant guinea pig with IGFs promotes placental transport and nutrient partitioning near term
AU - Sferruzzi-Perri, Amanda N.
AU - Owens, Julie A.
AU - Standen, Prue
AU - Taylor, Robyn L.
AU - Heinemann, Gary K.
AU - Robinson, Jeffrey S.
AU - Roberts, Claire T.
PY - 2007/3/1
Y1 - 2007/3/1
N2 - 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.
AB - 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.
KW - Fetal growth
KW - Glucose transport
KW - Insulin-like growth factor
KW - System A amino acid transport
UR - http://www.scopus.com/inward/record.url?scp=33947282207&partnerID=8YFLogxK
U2 - 10.1152/ajpendo.00320.2006
DO - 10.1152/ajpendo.00320.2006
M3 - Article
C2 - 17062842
AN - SCOPUS:33947282207
SN - 0193-1849
VL - 292
SP - E668-E676
JO - American Journal of Physiology-Endocrinology and Metabolism
JF - American Journal of Physiology-Endocrinology and Metabolism
IS - 3
ER -