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Cited by 28Pregnancy and preeclampsia studiesMuscle metabolism and nutritionBirth, Development, and Health

Ovine fetal leucine kinetics and protein metabolism during decreased oxygen availability

Milley, J. Ross·1998·American Journal of Physiology-Endocrinology and Metabolism
DOI 10.1152/ajpendo.1998.274.4.e618
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Abstract

The fetus depends on an uninterrupted supply of oxygen to provide energy, not only for basal metabolism but also for the metabolic costs of growth. By curtailing the metabolically expensive processes of protein turnover, the fetus could conserve energy when oxygen availability is limited. Therefore, this investigation was performed to find whether protein synthesis and breakdown are diminished during decreased fetal oxygen availability. Furthermore, if these conditions reduce fetal growth, protein synthesis should be affected more than breakdown so that protein accretion, an important component of fetal growth, also falls. In eight chronically prepared fetal lambs, we compared leucine kinetics (reciprocal pool model) during control conditions with measurements made during maternal hypoxia, a condition that limits fetal oxygen availability. Decreased fetal oxygen availability (−43%; P < 0.001) reduced fetal oxygen consumption (−16%; P < 0.01), as well as both the uptake of leucine across the placenta (−48%; P < 0.001) and its rate of decarboxylation (−30%; P < 0.001). Fetal protein synthesis decreased (−32%; P < 0.001) to a greater extent than proteolysis (−22%; P < 0.001). Consequently, fetal protein accretion, an important component of fetal growth, also decreased (−62%; P < 0.001). We calculate that the reduction in fetal protein synthesis and breakdown, both processes that require intracellular expenditure of ATP, decreased fetal energy needs sufficiently to account for most, if not all, of the decrease measured in fetal oxygen consumption.

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Crossref · 10.1152/ajpendo.1998.274.4.e618

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  • Consequently, there is little evidence for placental oxygen sparing in response to acute normobaric hypoxia in sheep, as may occur in the human placenta in response to the chronic hypoxia of high altitude.

    “Consequently, there is little evidence for placental oxygen sparing in response to acute normobaric hypoxia in the sheep (230, 263, 380), as may occur in the human placenta in response to the chronic hypoxia of high altitude (271).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [380]

  • Short-term hypoxic challenge induces changes in umbilical blood flow, with increases or decreases in flow immediately after the onset of maternal hypoxia depending on its severity.

    “This short-term type of hypoxic challenge also induces changes in umbilical blood flow, with increases or decreases in flow immediately after the onset of maternal hypoxia depending on its severity (380, 524).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [380]

  • In pregnant sheep, acute hypoxia for 4 h decreases the placental supply and fetal use of leucine in association with a general increase in amino-nitrogen availability in the fetal circulation and reduced rates of fetal protein synthesis and proteolysis.

    “In pregnant sheep, acute hypoxia for 4 h decreases the placental supply and fetal use of leucine in association with a general increase in amino-nitrogen availability in the fetal circulation and reduced rates of fetal protein synthesis and proteolysis (380).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [380]

  • Initially, fetal oxygen consumption decreases in line with placental delivery but then recovers to normal values despite sustained low delivery by increasing oxygen extraction.

    “Initially, fetal oxygen consumption decreases in line with placental delivery but then recovers to normal values despite the sustained low delivery by increasing oxygen extraction (230, 263, 380).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [380]

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Authors
Milley, J. R.
Affiliations
University of Utah (US)
Corresponding author
Milley, J. Ross
Venue
American Journal of Physiology-Endocrinology and Metabolism
Publisher
American Physiological Society
Published
1998-04-01
Volume
274
Issue
4
Pages
E618-E626
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
DOI
10.1152/ajpendo.1998.274.4.e618
OpenAlex
W2123051947
Cited by
28
References
33
Citations by year
2025: 1 · 2021: 1 · 2019: 1 · 2017: 2 · 2016: 2 · 2014: 3 · 2013: 2 · 2012: 2
FWCI
0.88
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (1r01hd027455-01)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01 HD27455)
Topics
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
Keywords
leucine kinetics, fetal hypoxia, maternal hypoxia, proteolysis, protein accretion, fetal growth, fetal oxygen consumption, fetal sheep, energy conservation
MeSH terms
Animals, Hypoxia, Biological Availability, Carbon Dioxide, Female, Fetal Blood, Fetus, Hematocrit, Hydrogen-Ion Concentration, Keto Acids, Kinetics, Leucine, Oxygen, Partial Pressure, Pregnancy, Proteins, Respiration, Sheep

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