Uteroplacental carbon substrate metabolism and oxygen consumption
after long term hypoglycemia in pregnant sheep.
Carver, Thomas D., William W. Hay, Jr.
Division of Perinatal Medicine and Research, Department of
Pediatrics, University of Colorado School of Medicine, Denver,
Colorado USA
APStracts 2:0067E, 1995.
Chronic maternal hypoglycemia leads to fetal growth restriction but
the effects on placental metabolism and its contribution to reduced
fetal growth have not been determined. To study these factors,
experiments were conducted in 7 normal, control [C] and 6 chronically
insulin-infused, hypoglycemic [H] pregnant sheep over the second half
of gestation to measure the effects of maternal and fetal
hypoglycemia (maternal: 2.0+/-0.2 mM H vs 3.6+/-0.1 mM C; fetal:
0.7+/-0.1 mM H vs 1.1+/-0.1 mM C) on placental metabolism of glucose,
other carbon substrates, and oxygen. Placental and fetal weight were
proportionately reduced in the hypoglycemic group (placental wt.:
258+/-18g H vs 376+/-18 g C, -31%; fetal wt: 2540+/-190g H, 3558+/
-230g C, -29%). Glucose uptake by the uterus was reduced in the
hypoglycemic group (0.10+/-0.01 mmol/min H vs 0.19+/-0.02 mmol/min
C); it was partitioned more to uteroplacental consumption (UPGC) and
less to transfer to the fetus (PGT): UPGC:PGT ratio 20.0+/-2.1 H,
13.5+/-1.2 C (P<0.05 for both). Metabolism of glucose by non
-oxidative and oxidative pathways (as estimated by the uteroplacental
lactate production to UPGC ratio and normal rates of placental oxygen
consumption) was not significantly changed in the hypoglycemic group.
Acetoacetate and [beta]-hydroxybutyrate net uptake and fructose
production rates were significantly reduced in the hypoglycemic
group, and there was no change in free fatty acid or amino acid
uptake rates. With acute return of maternal and fetal glucose
concentrations to normal, UPGC and PGT exceeded normal rates by about
25%. Thus, chronic reduced glucose supply to the uteroplacenta
produces a smaller placenta that uses glucose normally and in
preference to transfer to the fetus, demonstrating placental
metabolic autonomy at the expense of the fetus.
Received 15 September 1994; accepted in final form 22 March 1995.
APS Manuscript Number E382-4.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 19 April 1995.