Influence of placental 11β-hydroxysteroid dehydrogenase (11β-HSD) inhibition on glucose metabolism and 11β-HSD regulation in adult offspring of rats
References (33)
- et al.
Cloning and expression of rat cDNA encoding corticosteroid 11β-dehydrogenase
J Biol Chem
(1989) - et al.
The human gene for 11β-hydroxysteroid dehydrogenase structure, tissue distribution, and chromosomal localization
J Biol Chem
(1991) - et al.
Cloning and tissue distribution of the human 11β-hydroxysteroid dehydrogenase type 2 enzyme
Mol Cell Endocrinol
(1994) - et al.
Conversion of maternal cortisol to cortisone during placental transfer to the human fetus
Am J Obstet Gynecol
(1974) - et al.
Fetal nutrition and cardiovascular disease in adult life
Lancet
(1993) - et al.
Sex-specific effects of growth hormone on hepatic 11β-hydroxysteroid dehydrogenase activity and gene expression in hypothyroid rats
Life Sci
(1997) - et al.
Glucocorticoid exposure in utero: New model for adult hypertension
Lancet
(1993) - et al.
Effect of growth hormone, insulin and dexamethasone on 11β-hydroxysteroid dehydrogenase activity on a primary culture of rat hepatocytes
Life Sci
(1996) - et al.
Glucocorticoids regulate the induction of phosphoenolpyruvate carboxykinase (GTP) gene expression during diabetes
J Biol Chem
(1993) Insulin like growth factor binding proteins: More than just 1, 2, 3
Mol Cell Endocrinol
(1990)
Cloning, expression, and tissue distribution of the rat nicotinamide adenine dinucleotide-dependent 11β-hydroxysteroid dehydrogenase
Endocrinology
Cloning and production of antisera to human placental 11β-hydroxysteroid dehydrogenase type 2
Biochem J
Growth in utero, blood pressure in childhood and adult life, and mortality from cardiovascular disease
BMJ
Fetal and infant growth and impaired glucose tolerance at age 64
BMJ
Prenatal glucocorticoid exposure leads to offspring hyperglycaemia in the rat: Studies with the 11β-hydroxysteroid dehydrogenase inhibitor carbenoxolone
Diabetologia
Inhibition of 11β-hydroxysteroid dehydrogenase in pregnant rats and the programming of blood pressure in the offspring
Hypertension
Cited by (30)
Developmental toxicity and programming alterations of multiple organs in offspring induced by medication during pregnancy
2023, Acta Pharmaceutica Sinica BCitation Excerpt :Adverse conditions during pregnancy such as hypoxia and nutritional restriction can affect the expression of placental 11β-HSD2105, and the inhibitory effect of many drugs on the expression of 11β-HSD2 has also been proved. Studies have found that carbenoxolone, nicotine, caffeine, triclosan, and diethylstilbestrol can inhibit the activity of 11β-HSD2 in the placenta, which destroys the placental glucocorticoid barrier and causes fetal overexposure to maternal-derived glucocorticoids in utero106–110. Moreover, bortezomib, licorice, itraconazole, and posaconazole are all inhibitors of 11β-HSD2111,112, which may also damage the placental glucocorticoid barrier.
Dexamethasone programs lower fatty acid absorption and reduced PPAR-γ and fat/CD36 expression in the jejunum of the adult rat offspring
2021, Life SciencesCitation Excerpt :Experimental studies consistently suggest that the increased glucocorticoid production by pregnant rats exposed to stressful conditions plays a pivotal role in the programming of energy metabolism of the offspring [1,2].
Endocrine disruptors and other inhibitors of 11β-hydroxysteroid dehydrogenase 1 and 2: Tissue-specific consequences of enzyme inhibition
2016, Journal of Steroid Biochemistry and Molecular BiologyCitation Excerpt :In contrast, 11βHSD2 is strongly expressed in syncytiotrophoblast, the outler layer of a placenta that is the closest to maternal compartment [60,128]. It is widely accepted that 11βHSD2 in placenta creates a protective barrier to prevent a fetus against a maternal active glucocorticoids [60,126,129,130]. Also differences between cortisol levels in umbilical vein and umbilical artery showed that cortisol for the most part does not pass the placenta (changes in corticoid levels and levels of other steroids reviewed in [131]).
Role of the hypothalamic-pituitary-adrenal axis in developmental programming of health and disease
2013, Frontiers in NeuroendocrinologyCitation Excerpt :Application of glucocorticoids in the last week of gestation or throughout gestation leads to reduced beta-cell mass accompanied by decreased secretion of insulin in the fetal pancreas (Dumortier et al., 2011), which may be associated with hyperglycemia in adult offspring (Nyirenda et al., 1998). Suppression of 11β-HSD2 throughout pregnancy in rats reduces birth weight and causes hyperglycemia in adult offspring (Saegusa et al., 1999). Different from 11β-HSD2 that unidirectionally inactivates glucocorticoids, 11β-HSD1 is a bidirectional enzyme that acts predominantly as an oxidoreductase to regenerate active glucocorticoids from their inactive 11-keto derivatives.
Anti-diabetic and anti-adipogenic effects of a novel selective 11β-hydroxysteroid dehydrogenase type 1 inhibitor in the diet-induced obese mice
2012, European Journal of Pharmacology