Effects of insulin and hydrocortisone on lung tissue phosphatidyl choline and disaturated phosphatidyl choline in fetal rabbits in vivo

Patel, Daksha M.; Rhodes, Philip

doi:10.1007/bf00273915

Cited by 7 publications

(2 citation statements)

References 29 publications

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“…Glucose is an essential substrate for surfactant lipid synthesis. Insulin not only regulates glucose uptake to cells but also regulates surfactant synthesis [49]. The effect of different insulin and glucose concentrations on glucose uptake, glucose metabolism, and surfactant synthesis were examined in AEC2 cultures by Engle et al [50].…”

Section: Effects On Surfactant Phospholipid Compositionmentioning

confidence: 99%

Molecular Mechanisms of Maternal Diabetes Effects on Fetal and Neonatal Surfactant

2021

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Respiratory distress is a significant contributor to newborn morbidity and mortality. An association between infants of diabetic mothers (IDMs) and respiratory distress syndrome (RDS) has been well recognized for decades. As obesity and diabetes prevalence have increased over the past several decades, more women are overweight and diabetic in the first trimester, and many more pregnant women are diagnosed with gestational diabetes. Glycemic control during pregnancy can be challenging due to the maternal need for higher caloric intake and higher insulin resistance. Surfactant is a complex molecule at the alveolar air–liquid interface that reduces surface tension. Impaired surfactant synthesis is the primary etiology of RDS. In vitro cell line studies, in vivo animal studies with diabetic rat offspring, and clinical studies suggest hyperglycemia and hyperinsulinemia can disrupt surfactant lipid and protein synthesis, causing delayed maturation in surfactant in IDMs. A better understanding of the molecular mechanisms responsible for surfactant dysfunction in IDMs may improve clinical strategies to prevent diabetes-related complications and improve neonatal outcomes.

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Section: Effects On Surfactant Phospholipid Compositionmentioning

confidence: 99%

Molecular Mechanisms of Maternal Diabetes Effects on Fetal and Neonatal Surfactant

2021

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“…Inducing hyperinsulinemia by litter-size reduction decreased amniotic fluid surfactant in fetal rabbits (5). By contrast, inducing primary hyperinsulinemia in fetal rabbit or monkey in utero (6)(7)(8) failed to delay lung maturation. Furthermore, delayed lung maturation was observed in P-cytotoxic agent-induced animal models of diabetic pregnancy in which fetuses were devoid of reactional hyperinsulinism (9)(10)(11)(12)(13).…”

mentioning

confidence: 92%

Lung Maturation in the Hyperinsulinemic Rat Fetus

et al. 1987

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ABSTRACT. Hyperinsulinemic rat fetuses were obtained either by repeated in utero injections of long-acting insulin (resulting in fetal hypoglycemia) or by chronically infusing intravenous glucose to the mother (resulting in fetal hyperglycemia). Fetuses were examined at term. In insulininjected fetuses (n = IS), surfactant (S) fraction phosphatidylcholine (PC) and disaturated phosphatidylcholine (DSPC) were significantly decreased (3.6 f 0.1 nmol Pi/ mg tissue; p < 0.001 and 2.8 f 0.1 nmol/mg; p < 0.025, respectively) as compared with their saline-injected controls (4.8 f 0.2 and 3.3 f 0.1 nmol/mg, respectively, n-= 19). However, residual (R) fraction was unchanged, and there was no difference in whole-lung phospholipids (combined S and R fractions). These results are consistent with morphological data showing a lower lamellar body area per type I1 cell profile in insulin-injected fetuses as compared with their controls 11.41 f 0.13 pmZ (n = 72) versus 1.99 f 0.14 pm2 (n = 129) p < 0.011. Glycogen content was slightly higher in insulin-injected fetuses (18.5 f 1.0 pg/mg, n = 17) than in their controls (15.1 f 0.8 pg/mg, n = 18; p < 0.05). In the second model, changes in S fraction PC and DSPC were similar to those observed after insulininjections: 4.3 f 0.25 and 3.4 2 0.2 nmol Pi/mg in fetuses of glucose-infused rats (n = 10) versus 5.7 f 0.45 and 4.3 2 0.3 nmol Pi/mg, respectively, in controls (n = 10, p < 0.05). In addition, PG was also decreased (0.24 2 0.03 versus 0.40 f 0.04 nmol Pi/mg, n = 10; p < 0.01), and in contrast with insulin injections, reductions of DSPC and PG were detectable in whole lung. However, glycogen content was unchanged by glucose infusion (13.7 f 1.0 pg/ mg, n = 15 versus 14.0 f 1.1 pg/mg, n = 20 in controls).In both models, the phospholipid composition of material recovered by lung lavage was unchanged. Supported by lNSERM Grant PRC-135002 "Reproduction et Dtveloppement." 4The incidence of respiratory distress syndrome is increased in infants of diabetic mothers (1). This appears to result from a delayed maturation of the pulmonary surfactant system (2).A prominent feature of the fetus of diabetic mother is the association of hyperglycemia and reactional hyperinsulinemia (3). In vitro. an excess of insulin has been reueatedlv shown to dhay fetal ling maturation (reviewed in Ref, 2j. In vivb, however, the implication of hyperinsulinism in the mechanisms delaying lung maturation remains up to now an unsolved question. The maturational response of fetal lamb lungs to cortisol (4) was inhibited by chronic hyperglycemia and secondary hyperinsulinemia. Inducing hyperinsulinemia by litter-size reduction decreased amniotic fluid surfactant in fetal rabbits (5). By contrast, inducing primary hyperinsulinemia in fetal rabbit or monkey in utero (6)(7)(8) failed to delay lung maturation. Furthermore, delayed lung maturation was observed in P-cytotoxic agent-induced animal models of diabetic pregnancy in which fetuses were devoid of reactional hyperinsulinism (9-13). Both the latter approaches sug...

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Varying brain insulin concentrations differentially regulate the fetal brain insulin receptor

Devaskar

Karycki

Devaskar

1986

Biochemical and Biophysical Research Communications

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Effects of insulin and hydrocortisone on lung tissue phosphatidyl choline and disaturated phosphatidyl choline in fetal rabbits in vivo

Cited by 7 publications

References 29 publications

Molecular Mechanisms of Maternal Diabetes Effects on Fetal and Neonatal Surfactant

Molecular Mechanisms of Maternal Diabetes Effects on Fetal and Neonatal Surfactant

Lung Maturation in the Hyperinsulinemic Rat Fetus

Varying brain insulin concentrations differentially regulate the fetal brain insulin receptor

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