Effects of maternal insulin or glucose infusion on the fetus: Study on lung surfactant phospholipids, plasma myoinositol, and fetal growth in the rabbit

Plasma inositol levels in lithium‐treated manic‐depressives, schizophrenics and controls

“…Whether using an internal standard or not, some have obtained values of about 5 pg/ml (Clements et al, 1973;Hasegawa et al, 1988;Lewin et al, 1973;Servo et al, 1977) while another work (Pitkanen, 1972) documents 11.3 pg/ml (without using an internal standard), the same as found in the present work (using an internal standard).…”

Effect of myo-inositol on the glycerophospholipid composition of adult and fetal rat lung tissue

“…Although that investigation was performed employing type II pneumonocytes isolated from adult rats, it was shown in another investigation that, at least in the rabbit, the characteristics of myo-inositol uptake by slices of adult and fetal lung are very similar [3]. The present findings also complement the observation that when insulin was infused into pregnant rabbits the concentrations of glucose, insulin, and myo-inositol in fetal serum were decreased in association with the production by the fetus of a lung surfactant enriched in PG [15]. We speculate that myo-inositol may be involved also in the delayed appearance of PG in the lung surfactant of the human fetus in pregnancies complicated by diabetes mellitus.…”

“…During lung development in the human and in other species, the PG content of surfactant rises with a concomitant fall in phosphatidylinositol (PI) content. It has been proposed that the relative rates of synthesis of PI and PG for surfactant may be influenced by the availability of myo-inositol in the lung [3,15]. In many tissues, the limited amount of CDP-diacylglycerol that is present likely restricts the biosynthesis of both PI and PG and it has been observed in vitro that the metabolic fate of CDPdiacylglycerol is influenced by the extracellular concentration of myo-inositol [8,10,11].…”

Intrauterine growth restriction delays surfactant protein maturation in the sheep fetus

“…For example, glucose infusion in the fetal sheep with a concomitant increase in insulin had a biphasic effect on surfactant phosphatidylcholine content with an increase in midgestation and an inhibition of the normal rise in late gestation, which correlated with a reduction in lung stability (46). Intravenous insulin infusion during late gestation in pregnant rabbits resulted in decreased fetal serum glucose and insulin and improved survival of prematurely delivered fetuses and correlated with an increase in the quantity and quality of the lavagable surfactant phospholipid content (19). On the other hand, glucose infusion in the mother resulted in fetal hyperinsulinemia and hyperglycemia and no detectable difference in alveolar lavage phospholipids (19).…”

“…Intravenous insulin infusion during late gestation in pregnant rabbits resulted in decreased fetal serum glucose and insulin and improved survival of prematurely delivered fetuses and correlated with an increase in the quantity and quality of the lavagable surfactant phospholipid content (19). On the other hand, glucose infusion in the mother resulted in fetal hyperinsulinemia and hyperglycemia and no detectable difference in alveolar lavage phospholipids (19). As fetal hyperinsulinemia associated with maternal diabetes is associated with a reduction in SP-A protein in amniotic fluid (42) and an increased risk of developing RDS in the newborn, it has been hypothesized that insulin inhibits type II cell differentiation.…”