Effect of Dexamethasone on Lipoprotein Lipase Activity of Fetal Rat Lung

Abstract

Dexamethasone was administered by continuous subcutaneous infusions (16 μg/kg/h) to pregnant rats from day 16 of gestation. Administration of the hormone markedly affected maternal and fetal weight gain, fetal lung:body weight ratio and lipoprotein lipase activity of the lung. Cumulative maternal weight gain from days 15–21 of gestation was 80 ± 4.0 g in control and 30 ± 10 g in dexamethasone-treated rats. Fetal weight at 22 days of gestation and 1 day after birth was 5.5 ± 0.39 and 8.6 ± 0.30 in control and 4.65 ± 0.26 and 5.9 ± 0.34 in dexamethasone-treated rats. The ratio of lung weight to body weight was lower throughout the last 5 days of gestation in dexamethasone-treated than in control rats. Dexamethasone administration led to a 2- to 3-fold increase in lipoprotein lipase activity levels in fetal rat lung at 19 and 20 days’ gestation and prevented the decline in enzyme activity shortly before birth. Stimulation of fetal lung lipoprotein lipase activity suggests that increased uptake of triglyceride-fatty acids by the lung could be a contributory factor to corticosteroid-enhanced surfactant synthesis.

Growth, Elastin Concentration, and Collagen Concentration of Perinatal Rat Lung: Effects of Dexamethasone

“…The depression in total DNA content in the lungs of dexamethasone-exposed fetuses was considerable and reached a nadir of 60% at birth and on postnatal day 5 (not shown). The fetal lung appears particularly sensitive to the growth inhibitory effect of exogenous glucocorticoids which is in accord with previous observations (4,5) and is consistent with a high concentration of glucocorticoid receptors in the fetal lung (25). In contrast to lung weight and body weight which remained significantly lower in dexamethasone-treated rats until postnatal day 15 ( Fig.…”

“…The increase in fetal body weight and lung weight between day 18 of gestation and postnatal day 30 is substantial (5). Major structural transformations of the lungs take place during this period (20,21).…”

“…bovine serum albumin Exogenous glucocorticoids accelerate fetal lung maturation in many species including humans (1) and rats (2) and are used to advance lung maturation in the human fetus at risk of preterm delivery. Inhibition of lung growth after prenatal exposure to glucocorticoids has been observed in rabbits (3), rats (4,5 ) , and monkeys (6) and has given rise to concern for the human fetus exposed to such therapy.…”

Effects of Prenatal Treatment with Betamethasone,L-Carnitine, or Betamethasone-L-Carnitine Combinations on the Phosphatidylcholine Content and Composition of the Foetal and Maternal Rat Lung

“…However, a considerable number of infants fail to respond to this therapy (16). The concept that glucocorticoids only trigger receptors on foetal lung fibroblasts and/or type II cells to induce synthesis of surfactant lipid and protein components has been judged much too simplistic, especially since glucocorticoids cause foetal growth retardation in rabbit (18) and rat foetuses (19).…”

On the evolution of the pulmonary alveolar lipofibroblast

“…However, their functional relevance to the alveolus was not determined for two more decades, though their cytoprotective nature was suggested by comparative studies of Frank et al (16), who described the association between the LIFs and their putative role in overall antioxidant protection. These physiologic studies were paralleled by biochemical studies of triglyceride metabolism conducted by Mostello et al (17). The breakthrough in understanding the functional nature of these cells in lung alveolar physiology came with the co-culture of LIFs pre-labeled with radiolabeled triglyceride and naïve ATIIs, resulting in active uptake of the triglyceride by the ATIIs, and their subsequent robust incorporation into surfactant phospholipid by these cells (10), termed Neutral Lipid Trafficking.…”