Abstract
Mouse fetuses from the genetic diabetic mouse are macrosomic with increased body, lung and placenta weights and have abnormal carbohydrate metabolism with increased liver and placenta glycogen content. We studied the effect of increased glucose availability and utilization on lung growth and maturation in these fetuses at 18 days gestation (term±19). Phospholipid synthesis in lung slices was measured as 3H-choline incorporation into phosphatidylcholine (PC) and disaturated PC (SPC) and 14C-glycerol incorporation into phosphatidylglyoerol (PG) and phoaphatidylinositol (PI). The diabetic fetuses had significantly higher SPC synthesis than controls (881±65 vs 520±33 CPM/mg prot; mean±SE; p<.001) but significantly lower PG synthesis (212±26 Vs 327±35 CPM/mg prot; mean±SE; p<.02), with a lower 14C-PG/14C-PI ratio (1.81±.18 vs 3.17±.14; mean±SE; p<.001). Diabetic fetal lungs were morphologically less mature than controls, as shown by a significantly decreased air space density (.27±.01 vs .43±.02; mean±SE; p<.001) and alveolar epithelial cell/total tissue ratio (.54±.02 vs .66±.03; mean±SE; p<.01). Increased SPC synthesis in diabetic fetal lung may reflect the enhanced lung growth resulting in macrosomia. Lung maturation may be represented more specifically by PG synthesis, the PG/PI ratio, and morphologic indices, all of which were decreased in diabetic fetuses. Thus enhanced growth appears to coincide with delayed maturation. Further studies with this model of genetic diabetes will help clarify the mechanisms causing enhanced growth and delayed lung maturation in the infant of a diabetic mother.
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Lawrence, S., Nielsen, H. DELAYED FETAL LUNG MATURATION IN THE DIABETIC MOUSE. Pediatr Res 21 (Suppl 4), 217 (1987). https://doi.org/10.1203/00006450-198704010-00304
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DOI: https://doi.org/10.1203/00006450-198704010-00304