Inhibition of Surfactant Production by Insulin in Fetal Rabbit Lung Slices

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Incorporation of labeled glucose and fatty acid residues into saturated phosphatidylcholine was significantly reduced in lung slices from 27.5 days of gestation fetal rabbits during 90 min incubation in the presence of 100 μU/ml insulin. When 14C-glucose was used as substrate, incorporation into both phosphatidylcholine and saturated phosphatidylcholine was reduced by insulin. This occurred despite an increase in overall glucose utilization by the lung from 11.3 ± 3.9 to 16.3 ± 5.2 nmole/g tissue in the presence of insulin (P < 0.05). A decrease in incorporation of fatty acid residues into saturated phosphatidylcholine was also observed when 14C-paImitate was used as substrate, from 102 ± 4 to 90 ± 5 nmole palmitate/g tissue (P < 0.01). In the presence of insulin, there were significant reductions of both substrates appearing in lysophosphatidylcholine, a precursor of saturated phosphatidylcholine. There was no significant change in incorporation of glucose residues into glycogen or lactate under these conditions.


Hyperinsulinemia appears to be responsible for respiratory distress syndrome (RDS) in infants of diabetic mothers (IDM) and infants of gestational diabetic mothers (IGDM). Control of the maternal diabetic state to a degree which inhibits development of fetal hyperinsulinism reduces the incidence of RDS in IDM and IGDM by removing excess quantities of the factor, insulin, that is responsible for inhibition of surfactant production.

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