<i>In Utero</i>Regulation of Rhesus Monkey Fetal Adrenals: Effects of Dexamethasone, Adrenocorticotropin, Thyrotropin-Releasing Hormone, Prolactin, Human Chorionic Gonadotropin, and α-Melanocyte-Stimulating Hormone on Fetal and Maternal Plasma Steroids*

Walsh, Scott W.; Norman, Reid L.; Novy, Miles J.

doi:10.1210/endo-104-6-1805

Cited by 85 publications

(21 citation statements)

References 32 publications

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“…DEX treatment elicited an acute reduction in maternal plasma cortisol titers, directly in line with what has been reported several times in rhesus macaques (20,21,47,48) and reflecting treatment efficacy in terms of HPA-negative feedback (4), albeit in the circulation of the pregnant female rather than the fetuses. There was no effect of either EDEX or LDEX on the weight of the female, which included the fetoplacental unit; in the rhesus macaque, there is no effect of GCs on fetal body weight after cesarean delivery (20,21,24).…”

Section: Discussionsupporting

confidence: 83%

Effects of Prenatal Dexamethasone Treatment on Postnatal Physical, Endocrine, and Social Development in the Common Marmoset Monkey

Hauser¹,

Dettling-Artho²,

Pilloud³

et al. 2007

Endocrinology

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The prophylactic treatment of diagnosed preterm delivery with synthetic glucocorticoids, such as dexamethasone (DEX), is commonplace. Long-term effects of such treatment are not well understood. In the present study, we exposed pregnant common marmosets (Callithrix jacchus), small-bodied monkeys that are therefore advantageous for long-term primate studies, to daily repeated DEX (5 mg/kg orally) either during early (d 42-48) or late (d 90-96) pregnancy (gestation period of 144 d). Relative to control, we investigated DEX effects in terms of maternal endocrinology (plasma cortisol and estrogen titers) and offspring physical growth, plasma and urinary ACTH and cortisol titers, and social and maintenance behaviors from birth to weaning. Both DEX treatments resulted in markedly reduced maternal plasma cortisol titers during treatment and reduced estimated gestation period. Both treatments were without effects on neonate morphometric measurements and basal hypothalamic-pituitary-adrenal axis activity. Early DEX treatment resulted in increased infant body weight at postnatal d 56 and 84, co-occurring at the behavioral level with increased time spent in eating solid food, a mobile state, solitary play, and exhibiting tail hair piloerection. The constellation of physical and behavioral effects of early DEX suggests interesting parallels with the human metabolic syndrome, providing primate support that the latter is causally associated with the fetal environment, including prenatal programming. This novel primate in vivo evidence for postnatal effects of prenatal synthetic glucocorticoid exposure indicates the importance of improved understanding of this acute clinical treatment in terms of its long-term effects on offspring well-being.

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Section: Discussionsupporting

confidence: 83%

Effects of Prenatal Dexamethasone Treatment on Postnatal Physical, Endocrine, and Social Development in the Common Marmoset Monkey

Hauser¹,

Dettling-Artho²,

Pilloud³

et al. 2007

Endocrinology

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“…It is generally believed that Dex and betamethasone cross the placenta more readily than the natural glucocorticoid ligands because they are not bound to transporter proteins in maternal blood, nor are they as easily converted to cortisone by placental enzymes like 11 beta-hydroxysteroid dehydrogenase (11b-HSD). Once in the fetal compartment, the drugs affect hormone secretion and the unique fetal zone of the adrenal, resulting in a reduction of cortisol, dehydroepiandrosterone (DHEA) and possibly other adrenal androgens [16,17]. Because DHEA is an important precursor of the estrogen produced by the placenta, its inhibition may also explain the decline in maternal estrogen levels during Dex treatment [18].…”

Section: Fetal/placenta/uterine Physiologymentioning

confidence: 99%

Developmental consequences of antenatal dexamethasone treatment in nonhuman primates

Coe

Lubach

2005

Neuroscience & Biobehavioral Reviews

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“…In the monkey, cortisol of maternal origin accounts for much of the hormone present in the fetal compartment through mid-gestation (7). At high levels, especially if administered to the mother at pharmacological doses, it exceeds the capacity of the fetus to convert the hormone to less active forms, such as cortisone, or to shunt it back across the placenta (8). Then there can be deleterious effects on organ development, especially for hormonesensitive glands like the thymus (9).…”

mentioning

confidence: 99%

Prenatal Stress Diminishes the Cytokine Response of Leukocytes to Endotoxin Stimulation in Juvenile Rhesus Monkeys

Coe

Kramer

Kirschbaum³

et al. 2002

The Journal of Clinical Endocrinology &Amp; Metabolism

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This study investigated whether exposing the fetal primate to repeated episodes of maternal stress would have long-lasting effects on the endotoxin-induced cytokine response and corticosteroid sensitivity of peripheral blood cells in juvenile animals. Pregnant rhesus monkeys were acutely aroused on a daily basis for 6 wk using an acoustical startle protocol, either early or late in the 24-wk pregnancy. To quantify cytokine responses and corticosteroid sensitivity in their offspring at 2 yr of age, whole blood cultures were stimulated with lipopolysaccharide and incubated with dexamethasone (DEX). TNFalpha and IL-6 levels were determined in the culture supernatants. The blood samples were collected from undisturbed monkeys under baseline conditions, as well as in an aroused state induced by a 2 h social separation. Juvenile monkeys from stressed pregnancies had significantly lower cellular cytokine responses compared with the undisturbed controls. When DEX was added to the cell cultures, it systematically inhibited TNFalpha and IL-6 production, bringing the values for control animals down into the range of the prenatally stressed animals. Lipopolysaccharide-induced cytokine production was also markedly suppressed by the experience of acute stress, reducing cytokine responses of controls to the levels found for prenatally disturbed monkeys under baseline conditions. Therefore, this study has demonstrated that prenatal disturbance can induce a lasting change in cytokine biology, which persists well beyond the fetal and infant stage. Further, these effects may be due to elevated hypothalamic-pituitary-adrenal activity in the prenatally stressed animals, because both DEX and acute arousal made the cells from control monkeys appear more similar to those from disturbed pregnancies.

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In UteroRegulation of Rhesus Monkey Fetal Adrenals: Effects of Dexamethasone, Adrenocorticotropin, Thyrotropin-Releasing Hormone, Prolactin, Human Chorionic Gonadotropin, and α-Melanocyte-Stimulating Hormone on Fetal and Maternal Plasma Steroids*

Cited by 85 publications

References 32 publications

Effects of Prenatal Dexamethasone Treatment on Postnatal Physical, Endocrine, and Social Development in the Common Marmoset Monkey

Effects of Prenatal Dexamethasone Treatment on Postnatal Physical, Endocrine, and Social Development in the Common Marmoset Monkey

Developmental consequences of antenatal dexamethasone treatment in nonhuman primates

Prenatal Stress Diminishes the Cytokine Response of Leukocytes to Endotoxin Stimulation in Juvenile Rhesus Monkeys

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