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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... ABSTRACTExperiments 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 >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.Journal of Endocrinology (1989) 120, 393–399 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Endocrinology Bioscientifica

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

Conliffe, P.; Mulay, S.
Journal of Endocrinology , Volume 120 (3) – Mar 1, 1989
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Publisher
Bioscientifica
Copyright
Copyright © 1989 The Authors. All Rights Reserved.
ISSN
0022-0795
eISSN
1479-6805
DOI
10.1677/joe.0.1200393
Publisher site
See Article on Publisher Site

Abstract

ABSTRACTExperiments 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 >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.Journal of Endocrinology (1989) 120, 393–399

Journal

Journal of Endocrinology – Bioscientifica

Published: Mar 1, 1989

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