Tissue and Serum Concentrations of Somatomedin-C/Insulin-Like Growth Factor I in Fetal Rats Made Growth Retarded by Uterine Artery Ligation

Vileisis, Rita A.; D’Ercole, A. Joseph

doi:10.1203/00006450-198602000-00006

Cited by 63 publications

(22 citation statements)

References 34 publications

(43 reference statements)

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“…The changes observed in IGF-I in this study are consistent with previous data evaluating changes in IGF-I in the growthretarded fetus and in early postnatal life (8)(9)(10)22). Fetal rat pups rendered growth-retarded by uterine artery ligation were found to have depressed serum and tissue levels of IGF-I when compared with controls (9).…”

Section: Resultssupporting

confidence: 81%

“…Similarly, 10-d-old rat pups deprived of calories for 24 h showed significant reductions in serum levels of IGF-I, although no significant effects on hepatic IGF-I concentrations were found (8). Our results show absolute plasma IGF-I values in control and intrauterine growth-retarded animals similar to those reported previously, although the hepatic concentrations were approximately 10-fold higher than those previously reported using similar methodology (9). This discrepancy may reflect inherent differences in hepatic IGF-I concentration induced by uterine artery ligation compared with maternal substrate deprivation.…”

Section: Resultssupporting

confidence: 71%

“…Fetal rat pups rendered growth-retarded by uterine artery ligation were found to have depressed serum and tissue levels of IGF-I when compared with controls (9). Similarly, 10-d-old rat pups deprived of calories for 24 h showed significant reductions in serum levels of IGF-I, although no significant effects on hepatic IGF-I concentrations were found (8).…”

Section: Resultsmentioning

confidence: 86%

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Insulin-Like Growth Factor I in Substrate-Deprived, Growth-Retarded Fetal Rats

1991

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ABSTRACF. Plasma, amniotic fluid, and tissue concentra-Control animals were allowed free access to both food and water. tions of IGF-I were examined in nutritionally deprived, Sampling was performed on d 2 1 in all animals, after intraperigrowth-retarded fetal rats to determine whether IGF-I toneal pentobarbital (45 mg/kg) administration. Midline lapaconcentration serves as a marker for nutritional status. rotomy incision was used to expose the uterine horns. Fetuses in Growth retardation was induced by 72 h of maternal fast-each horn were counted, and the two inferior fetuses of each ing. Twenty-three control and 17 growth-retarded fetuses horn were sampled to match the control and test group with were individually analyzed and compared. Plasma IGF-I regard to intrauterine location. A maximum of four fetuses per concentrations were significantly lower in test compared dam were analyzed to insure matching of uterine location bewith control animals (test 56.8 f 14.9, control 87.4 f 17.5 tween groups and to minimize any metabolic impact of the ng/mL, p < 0.01). Amniotic fluid IGF-I concentrations surgical procedure. Only those fetuses in whom results from all were not different (test 14.0 f 8.7, control 12.2 f 2.6 ng/ specimens were available were included in the analyses. The mL). IGF-I concentrations obtained from both placental sampling sequence was initiated by the removal of amniotic fluid and hepatic tissues were lower in test compared with with a 19-or 20-gauge 1-mL syringe. The fetus was then removed control animals [placenta: test 293 f 25 versus control 655 from its location in the uterine horn, and an axillary cutdown f 114 ng/g (p < 0.001); hepatic: test 173 k 38 versus was performed (15). Fetal blood was collected by heparinized control 230 f 51 ng/g ( p < 0.01)]. Reductions in fetal, capillary tube, placed on ice, and centrifuged for 15 min at 12 placental, and hepatic weights in test animals were more 000 X g. The fetus was separated from the placenta, and the closely related to changes in placental IGF-I concentration fetus, placenta, and then fetal liver were weighed. The placenta than to either plasma or hepatic IGF-I concentrations. We and liver were quickfrozen in liquid nitrogen. All samples were conclude that fetal plasma IGF-I is a valuable marker for stored at -80°C until analysis. After fetal sampling, a maternal intrauterine substrate deprivation and that the growth-venous plasma sample was obtained from the inferior vena cava retarded rat fetus is accurately identified and specifically just below the renal vein. Euthanasia was performed by means characterized by a low placental concentration of extract-of exsanguination after all samples had been obtained. Individual Analyses. IGF-I concentrations in maternal and fetal plasma and amniotic fluid were determined by RIA [National Institute Circulating concentrations of IGF-I are influenced by both of Diabetes and Digestive and Kidney Diseases somatomedin-C growth hormone and nutritional status (1-10). Although the antiserum (polyclonal) cod...

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Section: Resultssupporting

confidence: 81%

Section: Resultssupporting

confidence: 71%

Section: Resultsmentioning

confidence: 86%

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Insulin-Like Growth Factor I in Substrate-Deprived, Growth-Retarded Fetal Rats

1991

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“…Experimentally induced fetal growth retardation in several species has been associated with decreases in fetal IGF-I concentrations. Studies in the pregnant rat (20) and guinea pig (9) have demonstrated that chronic restriction of uterine blood flow results in a decrease in fetal IGF-I concentrations. Similarly in the fetal sheep a reduction in placental size by carunclectomy also results in a decrease in fetal IGF-I levels and in fetal wt (lo, 11, 21).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Maternal Starvation on Plasma Insulin-Like Growth Factor I Concentrations in the Late Gestation Ovine Fetus

et al. 1990

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ABSTRACT. In view of the suggested relationship between substrate availability, fetal growth and circulating fetal IGF-I concentrations, we investigated the effect of maternal starvation on plasma IGF-I levels in the late gestation ovine fetus. Ten fetuses aged 125-130 d gestation were sampled daily from indwelling arterial catheters. Ewes were starved for 72 h. Starvation was terminated with an intravenous infusion of 10% glucose to the ewe. Food was then replaced 4 h later. Fetal IGF-I concentrations fell from 176.1 2 15.2 ng/mL before starvation to 124.5 f 10.3 ng/mL after 72 h starvation (p < 0.05, n = 10). The fall in IGF-I concentrations was reversed by 4 h of maternal glucose infusion. In five fetuses, where samples were obtained 24 h after terminating the starvation, fetal IGF-I concentrations were comparable to those seen before starvation (180.0 + 37.7 ng/mL). This study demonstrates that acute maternal starvation causes a reversible decrease in fetal plasma IGF-I levels. These studies suggest that nutrient and in particular glucose availability is a significant determinant of fetal IGF-I secretion and support the hypothesis that IGF-I may play a role in the regulation of fetal growth. (Pediatr Res 27: 401-404, 1990) Abbreviations GH, growth hormoneThe role of IGF in fetal life remains speculative. However, limited evidence suggests that IGF-I may have an important role in the regulation of fetal growth. IGF-I levels in umbilical cord blood at delivery have been shown to correlate with birth wt in a number of species including the rat (1, 2), rabbit (3), sheep (4), cow (5), and man (6-8). Studies in the fetal guinea pig (9) and fetal sheep (10, 11) have demonstrated that chronic alterations in placental function leading to fetal growth retardation result in decreases in fetal IGF-I levels. Such studies suggest that substrate availability may play a role in regulating fetal IGF-I secretion and that IGF-I may be an endocrine regulator of fetal growth. T o further elucidate the role of nutritional factors in the acute regulation of fetal IGF secretion we investigated the effects of maternal starvation and refeeding on plasma IGF-I levels in the late gestation ovine fetus. MATERIALS AND METHODSAnimals and surgical procedures. Romney ewes time mated with Suffolk rams provided fetuses of known gestational ages for these studies. At 125-1 30 d gestation (term = 145 f 3 d) ewes were brought into the laboratory and allowed 4-5 to become acclimatized to laboratory conditions before undergoing surgery. Fetal vascular surgery was performed under sterile conditions using halothane anaesthetic. Vascular catheters were inserted into the fetal femoral artery and vein and into the maternal tarsal artery and vein to obtain regular blood samples. Fetus and mother were allowed 5 d postoperative recovery before commencing the experiment. Ewes were fed a mixture of chaffed hay, lucerne, and barley ad libitum with water freely available.Experimental protocol. Blood samples were collected in sterile preheparinized syringes...

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“…Clinically, most fetal growth retardation states are associated with inadequate supply of both oxygen and nutrients to the fetus. Experimental models of growth retardation have generally used either interference with placental function (2) or uterine blood flow (6,12,13) or limitation of maternal energy and protein intake to restrict fetal growth (5,7,14). We have used maternal hypoxia as a model for IUGR and have studied its effect on IGF and their binding proteins to clarify their role in retarded fetal growth.…”

mentioning

confidence: 99%