Fetal lung development in streptozotocin-induced experimental diabetes: Cytidylyl transferase activity, disaturated phosphatidyl choline and glycogen levels

Mulay, Shree; McNaughton, L.

doi:10.1016/0024-3205(83)90252-7

Cited by 13 publications

(17 citation statements)

References 26 publications

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“…We found that fetal lung immaturity in rats made dia¬ betic by streptozotocin (Mulay & McNaughton, 1983) was associated with a decrease in maternal and fetal glucocorticoid levels . Because fetal adrenals can make a significant contri¬ bution to maternal glucocorticoid levels (Châtelain, Dupouy & Allaume, 1980;Mulay et al 1982), the decrease in maternal corticosterone concentrations in diabetic rats could be due to an inhibition of fetal steroidogenesis.…”

Section: Introductionmentioning

confidence: 94%

“…The following agents were received as gifts: synthetic hACTH(l-39) (Dr J. Rittel, Ciba, Basel, Switzerland) and antisera against insulin (Dr Y. Patel, Department of Medicine, McGill University, Montreal, Canada Induction of diabetes and collection of samples Details of some aspects of the methods used in these studies have been described previously Mulay & McNaughton, 1983). Briefly, pregnant Sprague-Dawley rats (200-225 g) were purchased from Charles River (St Constant, Quebec, Canada); the morning following the mating was designated as day 0 of pregnancy.…”

Section: Hormones and Reagentsmentioning

confidence: 99%

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Effects of insulin, glucose and ACTH on corticosterone production by fetal adrenal cells from diabetic rats

Conliffe

Mulay²

1989

Journal of Endocrinology

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Experiments were carried out on Sprague-Dawley rats to determine whether changes in fetal corticosterone levels during maternal diabetes were caused by the accompanying fetal hyperinsulinaemia or fetal hyperglycaemia. Diabetes was induced by injecting streptozotocin (30-45 mg/kg, i.v.) on day 2 of gestation. Fetal adrenals were removed on day 20 of gestation and cultured. Streptozotocin caused moderate (blood glucose 14-22.5 mmol/l) to severe (blood glucose greater than 25 mmol/l) diabetes. Both moderate and severe diabetes caused a decrease in fetal body weights. Relative to non-diabetic controls, maternal and fetal plasma concentrations of corticosterone were higher in the severely and lower in the moderately diabetic rats. Corticosterone production by fetal adrenal cells from control and moderately diabetic rats was comparable, but cells from the severely diabetic animals produced significantly greater amounts of corticosterone than did control cells. Neither glucose (28 mmol/l) nor insulin (1 nmol/l) exerted significant effects on [3H]thymidine uptake or corticosterone production by fetal adrenal cells from non-diabetic, moderately diabetic or severely diabetic rats. Human ACTH (0.02-20 nmol/l) caused a concentration-dependent increase in corticosterone output of comparable magnitude by cells from all three groups of animals. These data suggest that fetal growth abnormalities during diabetic pregnancy are not directly related to changes in glucocorticoid levels and that changes in glucocorticoid levels are not caused by any direct action of fetal hyperinsulinaemia or hyperglycaemia on adrenal cells.

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Section: Introductionmentioning

confidence: 94%

Section: Hormones and Reagentsmentioning

confidence: 99%

Effects of insulin, glucose and ACTH on corticosterone production by fetal adrenal cells from diabetic rats

Conliffe

Mulay²

1989

Journal of Endocrinology

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“…In addition, due to its cellular uptake via glucose transporter 2, not found in the lung, streptozotocin itself unlikely causes any fetal lung toxicity [7,22] . Although this diabetes model in rats differs from human diabetic pregnancy in some parameters, like lack of fetal macrosomia, it is still considered to offer a useful model to study the effects of hyperglycemia on perinatal lung development [6,7,23] . High maternal glycemic levels, permanently exceeding 20 mmol/l in pregnant rats, are in fact associated with fetal lung developmental delay, hypoinsulinemia and microsomia [23,24] .…”

Section: Discussionmentioning

confidence: 99%

“…Although this diabetes model in rats differs from human diabetic pregnancy in some parameters, like lack of fetal macrosomia, it is still considered to offer a useful model to study the effects of hyperglycemia on perinatal lung development [6,7,23] . High maternal glycemic levels, permanently exceeding 20 mmol/l in pregnant rats, are in fact associated with fetal lung developmental delay, hypoinsulinemia and microsomia [23,24] . In line with these observations, the lung weight of the hyperglycemiaexposed rat pups in our study at day 14 was lower despite similar body weight, indicating disturbed pulmonary growth.…”

Section: Discussionmentioning

confidence: 99%

“…L ist of selected biological functions (gene ontology categories) for genes significantly changing in the 14-day-old neonatal rat lung exposed to gestational hyperglycemia cells with induction of maternal and fetal hyperglycemia and a variable degree of fetal insulin secretion [7,16,[22][23][24] . A direct effect of streptozotocin on developing fetal organs was avoided in our study by administering it before mating.…”

Section: Discussionmentioning

confidence: 99%

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Maternal Hyperglycemia Modifies Extracellular Matrix Signaling Pathways in Neonatal Rat Lung

et al. 2010

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Background: Maternal diabetes is associated with numerous adverse effects in fetal and neonatal organs, including the lungs. Objective: To investigate the effects of intrauterine hyperglycemia on neonatal lung biological signaling, we performed a microarray analysis in the lungs of four 14-day-old rat pups born to a hyperglycemic dam and in four age mate control pup lungs. Methods: Total RNA was isolated and cDNA was hybridized to the Illumina Sentrix® RatRef-12 BeadChip. A total of 22,000 genes were analyzed for expression profiles and functional gene clustering. Ten selected genes differentially expressed in microarray were additionally analyzed by the real-time polymerase chain reaction. Results: Two hundred twenty-seven genes were differentially expressed in neonatal rat lungs exposed to intrauterine hyperglycemia when compared to normoglycemic controls (fold change > 1.2, p < 0.001). Functional clustering analysis revealed increased expression in signaling pathways involved with extracellular matrix regulation. The most significantly downregulated functions were cell proliferation, extracellular region, cell adhesion and reactive oxygen species metabolism. Conclusion: We found significant hyperglycemia-induced gene expression alterations in neonatal rat pulmonary tissue which may interfere with lung growth and biological signaling pathways.

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Ballard¹

1986

Hormones and Lung Maturation

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Fetal lung development in streptozotocin-induced experimental diabetes: Cytidylyl transferase activity, disaturated phosphatidyl choline and glycogen levels

Cited by 13 publications

References 26 publications

Effects of insulin, glucose and ACTH on corticosterone production by fetal adrenal cells from diabetic rats

Effects of insulin, glucose and ACTH on corticosterone production by fetal adrenal cells from diabetic rats

Maternal Hyperglycemia Modifies Extracellular Matrix Signaling Pathways in Neonatal Rat Lung

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