Fetal and Amniotic Insulin-Like Growth Factor-I Supplements Improve Growth Rate in Intrauterine Growth Restriction Fetal Sheep

Eremia, Simona; Boo, Hendrina A. de; Bloomfield, Frank H.; Oliver, Mark; Harding, Jane E.

doi:10.1210/en.2006-1701

Cited by 60 publications

(56 citation statements)

References 37 publications

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“…This would be in line with previous results showing increased protein synthesis in muscle mass but not in liver, kidney or spleen in rats after IGF-I administration [53]. Similarly, both intra-amniotic and intravenous IGF-I administration increased body weight in intrauterine growth-restricted fetal sheep, whereas only intra-amniotic administration increased liver weight [61]. Neither the brain nor the spleen weights increased after IGF-I treatment, independent of administration regimen.…”

Section: Discussionsupporting

confidence: 91%

Safety aspects of longitudinal administration of IGF-I/IGFBP-3 complex in neonatal mice

Hellgren

Han

Wang

et al. 2011

Growth Hormone & IGF Research

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Section: Discussionsupporting

confidence: 91%

Safety aspects of longitudinal administration of IGF-I/IGFBP-3 complex in neonatal mice

Hellgren

Han

Wang

et al. 2011

Growth Hormone & IGF Research

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“…IGF-1 signaling in the ␤-cell overlaps significantly with insulin signaling and, therefore, could be hypothesized to increase insulin secretion and ␤-cell mass in the HG fetuses (38). Furthermore, chronic fetal IGF-1 infusions are not associated with fetal hypoxemia, as found in the HGϩI fetuses in the current study (21,37). However, at higher doses of IGF-1 circulating fetal insulin concentrations are decreased and acute IGF-1 infusions inhibit GSIS in adults (37,53).…”

Section: Discussionsupporting

confidence: 51%

Increased fetal insulin concentrations for one week fail to improve insulin secretion or β-cell mass in fetal sheep with chronically reduced glucose supply

Lavezzi

Thorn

O'Meara

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Maternal undernutrition during pregnancy and placental insufficiency are characterized by impaired development of fetal pancreatic β-cells. Prolonged reduced glucose supply to the fetus is a feature of both. It is unknown if reduced glucose supply, independent of other complications of maternal undernutrition and placental insufficiency, would cause similar β-cell defects. Therefore, we measured fetal insulin secretion and β-cell mass following prolonged reduced fetal glucose supply in sheep. We also tested whether restoring physiological insulin concentrations would correct any β-cell defects. Pregnant sheep received either a direct saline infusion (CON = control, n = 5) or an insulin infusion (HG = hypoglycemic, n = 5) for 8 wk in late gestation (75 to 134 days) to decrease maternal glucose concentrations and reduce fetal glucose supply. A separate group of HG fetuses also received a direct fetal insulin infusion for the final week of the study with a dextrose infusion to prevent a further fall in glucose concentration [hypoglycemic + insulin (HG+I), n = 4]. Maximum glucose-stimulated insulin concentrations were 45% lower in HG fetuses compared with CON fetuses. β-Cell, pancreatic, and fetal mass were 50%, 37%, and 40% lower in HG compared with CON fetuses, respectively (P < 0.05). Insulin secretion and β-cell mass did not improve in the HG+I fetuses. These results indicate that chronically reduced fetal glucose supply is sufficient to reduce pancreatic insulin secretion in response to glucose, primarily due to reduced pancreatic and β-cell mass, and is not correctable with insulin.

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“…Nutrient and anabolic hormonal manipulation of the IUGR fetus to challenge programmed changes in growth pathways has been attempted previously. The most promising results have come from chronic, low-dose IGF-I infusions into the fetus in terms of improving fetal organ growth (13). Acute amino acid infusion with a concurrent increase in fetal plasma insulin concentrations increased protein accretion rates in the IUGR fetus (10); however, chronic glucose supplementation to the IUGR fetus resulted in hypoxia and acidosis (47).…”

Section: Discussionmentioning

confidence: 99%

Acute supplementation of amino acids increases net protein accretion in IUGR fetal sheep

Brown

Rozance

Thorn

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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Placental insufficiency decreases fetal amino acid uptake from the placenta, plasma insulin concentrations, and protein accretion, thus compromising normal fetal growth trajectory. We tested whether acute supplementation of amino acids or insulin into the fetus with intrauterine growth restriction (IUGR) would increase net fetal protein accretion rates. Late-gestation IUGR and control (CON) fetal sheep received acute, 3-h infusions of amino acids (with euinsulinemia), insulin (with euglycemia and euaminoacidemia), or saline. Fetal leucine metabolism was measured under steady-state conditions followed by a fetal muscle biopsy to quantify insulin signaling. In CON, increasing amino acid delivery rates to the fetus by 100% increased leucine oxidation rates by 100%. In IUGR, amino acid infusion completely suppressed fetal protein breakdown rates but increased leucine oxidation rate by only 25%, resulting in increased protein accretion rates by 150%. Acute insulin infusion, however, had very little effect on amino acid delivery rates, fetal leucine disposal rates, or fetal protein accretion rates in CON or IUGR fetuses despite robust signaling of the fetal skeletal muscle insulin-signaling cascade. These results indicate that, when amino acids are given directly into the fetal circulation independently of changes in insulin concentrations, IUGR fetal sheep have suppressed protein breakdown rates, thus increasing net fetal protein accretion.

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Fetal and Amniotic Insulin-Like Growth Factor-I Supplements Improve Growth Rate in Intrauterine Growth Restriction Fetal Sheep

Cited by 60 publications

References 37 publications

Safety aspects of longitudinal administration of IGF-I/IGFBP-3 complex in neonatal mice

Safety aspects of longitudinal administration of IGF-I/IGFBP-3 complex in neonatal mice

Increased fetal insulin concentrations for one week fail to improve insulin secretion or β-cell mass in fetal sheep with chronically reduced glucose supply

Acute supplementation of amino acids increases net protein accretion in IUGR fetal sheep

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