AJP - Endocrinology and Metabolism, Vol 253, Issue 6 E616-E620, Copyright © 1987 by American Physiological Society
Hyperglycemia and hyperinsulinemia increase glucose utilization in fetal rat tissues
A. Leturque, J. P. Revelli, S. Hauguel, J. Kande and J. Girard
Centre de Recherche sur la Nutrition, Centre National de la Recherche Scientifique, Meudon-Bellevue, France.
In vivo measurement of glucose utilization by individual tissues of 19-day
rat fetuses have been performed using radioactive 2-deoxy-D-glucose
technique. In the basal state, glucose metabolic index was 13.6 +/- 0.5
ng.min-1.mg-1 for the whole fetus, 21 +/- 1 in the hindlimb muscles, 13 +/-
2 in the liver, and 16 +/- 2 in the brain, whereas the fetal heart had the
highest value: 62 +/- 5 ng.min-1.mg-1. To raise the fetal glycemia, the
basal maternal blood glucose concentration of 0.78 +/- 0.02 g/l was
elevated to 1.04 +/- 0.02 g/l by mean of hyperglycemic clamps. The fetal
hyperglycemia increased glucose metabolic index by 30-100% over basal
values in all the tissues tested except in the brain. To raise fetal
insulinemia, maternal euglycemic clamp with supraphysiological insulin
concentrations were performed, then a fraction (1%) of exogenous insulin
crossed the placenta. Fetal plasma insulin concentrations were thus
elevated to 180 +/- 32 and 255 +/- 23 microU/ml. The fetal heart increased
significantly its glucose metabolic index in response to the lower insulin
level. Glucose metabolic index in hindlimb muscles and liver was increased
by 50-100% for the highest insulin level, whereas the brain was unaffected
by exogenous insulin. We conclude that glucose metabolic index is
stimulated by physiological hyperglycemia in individual fetal tissues and
that fetal tissues (heart, liver, and muscle) are sensitive to exogenous
insulin.
