Hypoglycemia and the origin of hypoxia-induced reduction in human fetal growth
Abtract. Background: The most well known reproductive consequence of residence at high altitude (HA .2700 m) is reduction in fetal growth. Reduced fetoplacental oxygenation is an underlying cause of pregnancy pathologies, including intrauterine growth restriction and preeclampsia, which are more common at HA. Therefore, altitude is a natural experimental model to study the etiology of pregnancy pathophysiologies. We have shown that the proximate cause of decreased fetal growth is not reduced oxygen availability, delivery, or consumption. We therefore asked whether glucose, the primary substrate for fetal growth, might be decreased and/or whether altered fetoplacental glucose metabolism might account for reduced fetal growth at HA. Methods: Doppler and ultrasound were used to measure maternal uterine and fetal umbilical blood flows in 69 and 58 residents of 400 vs 3600 m. Arterial and venous blood samples from mother and fetus were collected at elective cesarean delivery and analyzed for glucose, lactate and insulin. Maternal delivery and fetal uptakes for oxygen and glucose were calculated. Principal Findings: The maternal arterial – venous glucose concentration difference was greater at HA. However, umbilical venous and arterial glucose concentrations were markedly decreased, resulting in lower glucose delivery at 3600 m. Fetal glucose consumption was reduced by .28%, but strongly correlated with glucose delivery, highlighting the relevance of glucose concentration to fetal uptake. At altitude, fetal lactate levels were increased, insulin concentrations decreased, and the expression of GLUT1 glucose transporter protein in the placental basal membrane was reduced. Conclusion/Significance: Our results support that preferential anaerobic consumption of glucose by the placenta at high altitude spares oxygen for fetal use, but limits glucose availability for fetal growth. Thus reduced fetal growth at high altitude is associated with fetal hypoglycemia, hypoinsulinemia and a trend towards lactacidemia. Our data support that placentally-mediated reduction in glucose transport is an initiating factor for reduced fetal growth under conditions of chronic hypoxemia.
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PLOS One
2010-01
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Subjects: | HIPOGLICEMIA, HIPOXIA-INDUCIDA, CRECIMIENTO FETAL, |
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oai:localhost:8080:123456789-81312020-09-23T18:16:59Z Hypoglycemia and the origin of hypoxia-induced reduction in human fetal growth Zamudio, Stacy Torricos, Tatiana Fik, Ewa Oyala, María Echalar, Lourdes Pullockaran, Janet Tutino, Emily Martin, Brittney Belliappa, Sonia Balanza, Elfride Illsley, Nicholas P HIPOGLICEMIA HIPOXIA-INDUCIDA CRECIMIENTO FETAL Abtract. Background: The most well known reproductive consequence of residence at high altitude (HA .2700 m) is reduction in fetal growth. Reduced fetoplacental oxygenation is an underlying cause of pregnancy pathologies, including intrauterine growth restriction and preeclampsia, which are more common at HA. Therefore, altitude is a natural experimental model to study the etiology of pregnancy pathophysiologies. We have shown that the proximate cause of decreased fetal growth is not reduced oxygen availability, delivery, or consumption. We therefore asked whether glucose, the primary substrate for fetal growth, might be decreased and/or whether altered fetoplacental glucose metabolism might account for reduced fetal growth at HA. Methods: Doppler and ultrasound were used to measure maternal uterine and fetal umbilical blood flows in 69 and 58 residents of 400 vs 3600 m. Arterial and venous blood samples from mother and fetus were collected at elective cesarean delivery and analyzed for glucose, lactate and insulin. Maternal delivery and fetal uptakes for oxygen and glucose were calculated. Principal Findings: The maternal arterial – venous glucose concentration difference was greater at HA. However, umbilical venous and arterial glucose concentrations were markedly decreased, resulting in lower glucose delivery at 3600 m. Fetal glucose consumption was reduced by .28%, but strongly correlated with glucose delivery, highlighting the relevance of glucose concentration to fetal uptake. At altitude, fetal lactate levels were increased, insulin concentrations decreased, and the expression of GLUT1 glucose transporter protein in the placental basal membrane was reduced. Conclusion/Significance: Our results support that preferential anaerobic consumption of glucose by the placenta at high altitude spares oxygen for fetal use, but limits glucose availability for fetal growth. Thus reduced fetal growth at high altitude is associated with fetal hypoglycemia, hypoinsulinemia and a trend towards lactacidemia. Our data support that placentally-mediated reduction in glucose transport is an initiating factor for reduced fetal growth under conditions of chronic hypoxemia. 2016-10-03T18:15:50Z 2016-10-03T18:15:50Z 2010-01 Article http://repositorio.umsa.bo/xmlui/handle/123456789/8131 en application/pdf PLOS One |
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HIPOGLICEMIA HIPOXIA-INDUCIDA CRECIMIENTO FETAL HIPOGLICEMIA HIPOXIA-INDUCIDA CRECIMIENTO FETAL |
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HIPOGLICEMIA HIPOXIA-INDUCIDA CRECIMIENTO FETAL HIPOGLICEMIA HIPOXIA-INDUCIDA CRECIMIENTO FETAL Zamudio, Stacy Torricos, Tatiana Fik, Ewa Oyala, María Echalar, Lourdes Pullockaran, Janet Tutino, Emily Martin, Brittney Belliappa, Sonia Balanza, Elfride Illsley, Nicholas P Hypoglycemia and the origin of hypoxia-induced reduction in human fetal growth |
description |
Abtract.
Background: The most well known reproductive consequence of residence at high altitude (HA .2700 m) is reduction in
fetal growth. Reduced fetoplacental oxygenation is an underlying cause of pregnancy pathologies, including intrauterine
growth restriction and preeclampsia, which are more common at HA. Therefore, altitude is a natural experimental model to study the etiology of pregnancy pathophysiologies. We have shown that the proximate cause of decreased fetal growth is not reduced oxygen availability, delivery, or consumption. We therefore asked whether glucose, the primary substrate for fetal growth, might be decreased and/or whether altered fetoplacental glucose metabolism might account for reduced fetal growth at HA.
Methods: Doppler and ultrasound were used to measure maternal uterine and fetal umbilical blood flows in 69 and 58
residents of 400 vs 3600 m. Arterial and venous blood samples from mother and fetus were collected at elective cesarean
delivery and analyzed for glucose, lactate and insulin. Maternal delivery and fetal uptakes for oxygen and glucose were
calculated.
Principal Findings: The maternal arterial – venous glucose concentration difference was greater at HA. However, umbilical
venous and arterial glucose concentrations were markedly decreased, resulting in lower glucose delivery at 3600 m. Fetal
glucose consumption was reduced by .28%, but strongly correlated with glucose delivery, highlighting the relevance of
glucose concentration to fetal uptake. At altitude, fetal lactate levels were increased, insulin concentrations decreased, and
the expression of GLUT1 glucose transporter protein in the placental basal membrane was reduced.
Conclusion/Significance: Our results support that preferential anaerobic consumption of glucose by the placenta at high
altitude spares oxygen for fetal use, but limits glucose availability for fetal growth. Thus reduced fetal growth at high
altitude is associated with fetal hypoglycemia, hypoinsulinemia and a trend towards lactacidemia. Our data support that placentally-mediated reduction in glucose transport is an initiating factor for reduced fetal growth under conditions of chronic hypoxemia. |
format |
Article |
topic_facet |
HIPOGLICEMIA HIPOXIA-INDUCIDA CRECIMIENTO FETAL |
author |
Zamudio, Stacy Torricos, Tatiana Fik, Ewa Oyala, María Echalar, Lourdes Pullockaran, Janet Tutino, Emily Martin, Brittney Belliappa, Sonia Balanza, Elfride Illsley, Nicholas P |
author_facet |
Zamudio, Stacy Torricos, Tatiana Fik, Ewa Oyala, María Echalar, Lourdes Pullockaran, Janet Tutino, Emily Martin, Brittney Belliappa, Sonia Balanza, Elfride Illsley, Nicholas P |
author_sort |
Zamudio, Stacy |
title |
Hypoglycemia and the origin of hypoxia-induced reduction in human fetal growth |
title_short |
Hypoglycemia and the origin of hypoxia-induced reduction in human fetal growth |
title_full |
Hypoglycemia and the origin of hypoxia-induced reduction in human fetal growth |
title_fullStr |
Hypoglycemia and the origin of hypoxia-induced reduction in human fetal growth |
title_full_unstemmed |
Hypoglycemia and the origin of hypoxia-induced reduction in human fetal growth |
title_sort |
hypoglycemia and the origin of hypoxia-induced reduction in human fetal growth |
publisher |
PLOS One |
publishDate |
2010-01 |
url |
http://repositorio.umsa.bo/xmlui/handle/123456789/8131 |
work_keys_str_mv |
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