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Am J Physiol Endocrinol Metab 264: E250-E256, 1993;
0193-1849/93 $5.00
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AJP - Endocrinology and Metabolism, Vol 264, Issue 2 E250-E256, Copyright © 1993 by American Physiological Society

ARTICLES

Exogenous substrate uptake by fetal lambs during reduced glucose delivery

J. R. Milley
Department of Pediatrics, University of Utah School of Medicine, Salt Lake City 84132.

Normally, metabolism of exogenous glucose accounts for one-half of the normal fetal metabolic rate. When fetal glucose delivery is restricted for 2 wk, endogenous production increases to maintain glucose use. Such increased glucose production must originate either from increased uptake of other exogenous substrates (lactate or amino acids) or from use of endogenous substrates (via glycogenolysis or gluconeogenesis). Our purpose was to find if exogenous fetal substrate uptake increased during decreased fetal glucose delivery. Catheters were placed in eight lamb fetuses under general maternal anesthesia, and the animals were allowed 6 days to recover. Umbilical venoarterial blood concentration differences of antipyrine (during fetal antipyrine infusion), glucose, lactate, amino nitrogen-containing substances, and oxygen were measured before and after fetal glucose delivery was diminished by 3 h of maternal insulin infusion (5-10 mU.kg-1.m-1). Fetal substrate uptakes and substrate/oxygen quotients (i.e., the proportion of oxidative metabolism supported by complete oxidation of each exogenous substrate) were calculated. No increase occurred in the uptake of other exogenous substrates during deficient glucose delivery. Because even complete oxidation of all exogenous substrates did not meet fetal oxidative requirements, the fetus must oxidize endogenous substrates. If such a pattern of substrate use were to continue, fetal growth retardation would result.


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T. Maeda and B. J. Koos
Adenosine A1 and A2a receptors modulate insulinemia, glycemia, and lactatemia in fetal sheep
Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2009; 296(3): R693 - R701.
[Abstract] [Full Text] [PDF]


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