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Division of Neonatology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah 84132
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.
fetal growth; intrauterine growth retardation; protein synthesis; proteolysis
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