We have examined whether glucose supply to fetal sheep erythrocytes limits the rate of 20α-reduction of progesterone in blood and as such is associated with the progressive loss of 20α-hydroxysteroid dehydrogenase activity which has been observed from 30 days before term.
Enzyme activity in erythrocytes depleted of glucose by washing was regained in the presence of at least 0·167 mmol glucose/l. The cofactor NADPH was necessary to support the reaction in lysed cells. Addition of glucose to whole blood diluted 20-fold for assay of 20α-hydroxysteroid dehydrogenase did not increase the rate of reaction. Infusion of dextrose to increase fetal plasma glucose concentrations had no effect on 20α-hydroxysteroid dehydrogenase activity. Over the period from 114 to 137 days of gestation, both dextrose- and saline-infused fetuses showed a decline in enzyme activity from a combined mean of 1·45 ± 0·21 (s.e.m.) to a mean of 0·78 ± 0·18 μmol/ml erythrocytes per h. Fetal leucocytes did not contribute significantly to the activity of 20α-hydroxysteroid dehydrogenase in whole blood.
The rate of 20α-reduction of progesterone in the blood of eight fetuses with indwelling carotid catheters declined from 2·31 ± 0·09 μmol/ml erythrocytes per h at 90–95 days of gestation to 0·73 ± 0·04 μmol/ml per h at 141–145 days. However, a consistent decline was only observed after 116–120 days. The apparent equilibrium position for progesterone reduction to 20α-dihydroprogesterone varied between 83·9 ± 1·8 and 65·7 ± 4·2%.
Thus, it appears that the decline in 20α-hydroxysteroid dehydrogenase activity which occurs in whole blood of sheep fetuses during the last 30 days of gestation is due to dilution of the fetal erythrocytes with adult-type erythrocytes rather than development of limiting concentrations of plasma glucose.
J. Endocr. (1984) 101, 131–139
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