Effects of prenatal betamethasone administration on leptin and adiponectin concentrations in maternal and fetal circulation

Marinoni, Emanuela; Letizia, Claudio; Ciardo, Francesca; Corona, Giovanna; Mangino, Massimo; Iorio, Raffaele

doi:10.1016/j.ajog.2008.02.047

Cited by 13 publications

(13 citation statements)

References 29 publications

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“…Some studies have demonstrated that glucocorticoids inhibit fetal growth when administered during later stages of gestation in sheep, rats, nonhuman primates, and humans33 while, similar to our observations, other studies report no adverse effects of antenatal glucocorticoid on fetal weight in human pregnancy 34. Our findings agree with several human reports showing that prenatal glucocorticoids do not lower birth weight 35-37. Discrepancies between studies in both humans and non-human primates (regarding fetal weight changes after glucocorticoid administration) may reflect usage of dexamethasone, and not betamethasone.…”

Section: Discussionsupporting

confidence: 92%

“…Our data show that the prolonged elevation of leptin level after betamethasone treatment is not associated with changes in IGF, glucose, cholesterol, or GH status. The clinical observations of Marinoni et al 37 reinforce the direct application of our own findings to human pregnancy. The baboon is a promising model to study key questions related to the metabolic changes associated with prenatal glucocorticoid exposure.…”

Section: Resultssupporting

confidence: 85%

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The Prolonged Effect of Repeated Maternal Glucocorticoid Exposure on the Maternal and Fetal Leptin/Insulin-like Growth Factor Axis in Papio species

Schlabritz‐Loutsevitch

López-Alvarenga

Comuzzie

et al. 2009

Reprod. Sci.

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Section: Discussionsupporting

confidence: 92%

Section: Resultssupporting

confidence: 85%

The Prolonged Effect of Repeated Maternal Glucocorticoid Exposure on the Maternal and Fetal Leptin/Insulin-like Growth Factor Axis in Papio species

Schlabritz‐Loutsevitch

López-Alvarenga

Comuzzie

et al. 2009

Reprod. Sci.

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“…Although there is little doubt about the functional significance of leptin in pregnancy, it is less clear how leptin expression and secretion are regulated in the placenta. Studies have shown that proinflammatory cytokines, estrogen, glucocorticoids, and activation of the cAMP pathway are all inducers of leptin synthesis in placental syncytiotrophoblasts (Chardonnens et al 1999, Coya et al 2001, Nuamah et al 2004, Marinoni et al 2008, Gambino et al 2010. Recently it was demonstrated that exogenous hCG stimulated leptin expression in human placental cell line as well as in human placental explants (Maymo et al 2009), which is confirmed by the findings in this study that exogenous hCG or activation of cAMP pathway with forskolin and db cAMP induced leptin production in primary placental syncytiotrophoblasts.…”

Section: Discussionmentioning

confidence: 99%

Cross talk between cAMP and p38 MAPK pathways in the induction of leptin by hCG in human placental syncytiotrophoblasts

Li²,

Ni³

et al. 2011

Reproduction

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Leptin produced by the placental syncytiotrophoblasts participates in a number of processes in pregnancy including implantation, proliferation of the cytotrophoblasts, and nutrient transfer across the placenta. Despite the functional significance of leptin in pregnancy, the regulation of leptin synthesis is poorly understood in human placental syncytiotrophoblasts. In this study, we investigated the role of endogenous human chorionic gonadotropin (hCG) in the regulation of leptin production as well as the underlying mechanism involving the cross talk between cAMP and p38 mitogen-activated protein kinase (MAPK) pathways. We found that neutralization of endogenous hCG with its antibody dose dependently decreased leptin mRNA level and secretion, whereas exogenous hCG increased leptin mRNA level and secretion. Activation of the cAMP pathway with dibutyryl cAMP (db cAMP) or forskolin recapitulated the stimulatory effect of hCG on leptin expression. Inhibition of protein kinase A with H89 not only reduced the basal leptin expression but also attenuated the induced leptin expression by hCG. Treatment of the syncytiotrophoblasts with db cAMP and hCG phosphorylated p38 MAPK. Inhibition of p38 MAPK with SB203580 not only reduced the basal leptin production but also attenuated the leptin-induced production by both hCG and db cAMP. These data suggest that endogenous hCG plays a significant role in maintaining leptin production in human placental syncytiotrophoblasts, and this effect involves a cross talk between cAMP and p38 MAPK pathways.

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“…For instance, perinatal glucocorticoids, in rodents and humans, can lead to elevations in plasma leptin (Bruder et al, 2005; Marinoni et al, 2008). Given what we know about the sensitivity of the developing hypothalamic connectivity to circulating leptin at this time, it is highly likely this glucocorticoid-mediated increase in leptin interferes with the normal leptin-induced establishment of connections between the ARC, PVN, dorsomedial nucleus of the hypothalamus (DMH), and lateral hypothalamus (LH).…”

Section: Mechanisms Of Early Life Influence On Hpa Axis Functionmentioning

confidence: 99%

“…There is no doubt that several current perinatal treatments, while crucial for their immediate purpose, have far-reaching side-effects on systems such as the HPA axis and feeding circuitry. For instance, synthetic glucocorticoid, administered prenatally to assist in lung development, may elevate plasma leptin (Marinoni et al, 2008), stimulate epigenetic modifications in GR and elevate 11βHSD2 (Clifton et al, 2006). Similarly, the current practice of intensively feeding premature and small for gestational age babies to accelerate brain and lung development has the negative side-effect of predisposing these babies to long-term excess weight gain (Ong et al, 2000; Stettler et al, 2005).…”

Section: Conclusion and Clinical Implicationsmentioning

confidence: 99%

Eating behavior and stress: a pathway to obesity

2014

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Stress causes or contributes to a huge variety of diseases and disorders. Recent evidence suggests obesity and other eating-related disorders may be among these. Immediately after a stressful event is experienced, there is a corticotropin-releasing-hormone (CRH)-mediated suppression of food intake. This diverts the body’s resources away from the less pressing need to find and consume food, prioritizing fight, flight, or withdrawal behaviors so the stressful event can be dealt with. In the hours following this, however, there is a glucocorticoid-mediated stimulation of hunger and eating behavior. In the case of an acute stress that requires a physical response, such as a predator-prey interaction, this hypothalamic-pituitary-adrenal (HPA) axis modulation of food intake allows the stressful event to be dealt with and the energy used to be replaced afterward. In the case of ongoing psychological stress, however, chronically elevated glucocorticoids can lead to chronically stimulated eating behavior and excessive weight gain. In particular, stress can enhance the propensity to eat high calorie “palatable” food via its interaction with central reward pathways. Activation of this circuitry can also interact with the HPA axis to suppress its further activation, meaning not only can stress encourage eating behavior, but eating can suppress the HPA axis and the feeling of stress. In this review we will explore the theme of eating behavior and stress and how these can modulate one another. We will address the interactions between the HPA axis and eating, introducing a potential integrative role for the orexigenic hormone, ghrelin. We will also examine early life and epigenetic modulation of the HPA axis and how this can influence eating behavior. Finally, we will investigate the clinical implications of changes to HPA axis function and how this may be contributing to obesity in our society.

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Effects of prenatal betamethasone administration on leptin and adiponectin concentrations in maternal and fetal circulation

Cited by 13 publications

References 29 publications

The Prolonged Effect of Repeated Maternal Glucocorticoid Exposure on the Maternal and Fetal Leptin/Insulin-like Growth Factor Axis in Papio species

The Prolonged Effect of Repeated Maternal Glucocorticoid Exposure on the Maternal and Fetal Leptin/Insulin-like Growth Factor Axis in Papio species

Cross talk between cAMP and p38 MAPK pathways in the induction of leptin by hCG in human placental syncytiotrophoblasts

Eating behavior and stress: a pathway to obesity

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