Stimulation of Rabbit Fetal Lung Phospholipids

275+72 mg/dl, P < 0.05) and fetal glucose (64+6 vs. 274±47 mg/dl, P < 0.001) compared with salineinjected diabetic (D) mothers. Reduction of fetal insulin levels was also associated with maternal DIMIT therapy in diabetic rabbits (56±5 (D) vs. 24±4 ,uU/ml, P < 0.001). Maternal diabetes resulted in significant reduction of fetal lung weight (370+20 vs. 520±30 mg, P < 0.005) and lung protein content (6.5±0.7 vs. 8.7±0.7 mg/gm, P < 0.005), which were restored to normal in offspring of DIMIT-treated diabetic rabbits. Maternal DIMIT administration caused significant reduction in fetal lung glycogen content in control (62±5.8 vs. 25±5.9 ,ug/mg protein, P < 0.001) and diabetic (56±7 vs. 34±5 gg/mg protein, P < 0.02) offspring. Whereas maternal diabetes was associated with reduction of all major phospholipid species in fetal lung-comprising surfactant, these were restored with DIMIT therapy. Dr. Neufeld and Dr. Melmed are both recipients of Clinical Investigator Awards, National Institute of Arthritis, Metabolism and Digestive Diseases AM 00380 and AM 00906. Received for publication 21 August 1981 and in revised form 21 September 1981. J. Clin. Invest. (C The American Society for Clinical Investiga; The results demonstrate that short-term maternal administration of DIMIT in pregnant diabetic rabbits not only promotes fetal lung phospholipid synthesis, but also appears to ameliorate maternal hyperglycemia. Thus, DIMIT is ofpotential benefit in the management of diabetic pregnancy.