Corticosteroid-Binding Globulin Status at the Fetomaternal Interface During Human Term Pregnancy1

Benassayag, C.; Souski, Isabelle; Mignot, Thérèse-Marie; Robert, Brigitte; Hassid, J.; Duc-Goiran, P.; Mondon, Françoise; Rebourcet, R; Dehennin, L.; Nunez, Emmanuel A.; Ferré, Françoise

doi:10.1095/biolreprod64.3.812

Cited by 37 publications

(32 citation statements)

References 37 publications

(65 reference statements)

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“…CBG may be narrowly expressed in human tissues, with definite tissue expression demonstrated in hepatocytes and in placental syncytiotrophoblasts (24) where CBG may modulate glucocorticoid and progesterone tissue interactions (2). CBG has been reported in rodent adipose tissue by corticosterone binding but not gene expression (11,12), and this may represent circulating CBG from plasma taken into cells.…”

Section: Discussionmentioning

confidence: 99%

Greater replication and differentiation of preadipocytes in inherited corticosteroid-binding globulin deficiency

Joyner

Hutley

Bachmann

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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Glucocorticoids are pivotal for adipose tissue development. Rodent studies suggest that corticosteroid-binding globulin (CBG) modulates glucocorticoid action in adipose tissue. In humans, both genetic CBG deficiency and suppressed CBG concentrations in hyperinsulinemic states are associated with obesity. We hypothesized that CBG deficiency in humans modulates the response of human preadipocytes to glucocorticoids, predisposing them to obesity. We compared normal preadipocytes with subcultured preadipocytes from an individual with the first ever described complete deficiency of CBG due to a homozygous null mutation. CBG-negative preadipocytes proliferated more rapidly and showed greater peroxisome proliferator-activated receptor-γ-mediated differentiation than normal preadipocytes. CBG was not expressed in normal human preadipocytes. Glucocorticoid receptor number and binding characteristics and 11β-hydroxysteroid dehydrogenase activity were similar for CBG-negative and normal preadipocytes. We propose that the increased proliferation and enhanced differentiation of CBG-negative preadipocytes may promote adipose tissue deposition and explain the obesity seen in individuals with genetic CBG deficiency. Furthermore, these observations may be relevant to obesity occurring with suppressed CBG concentrations associated with hyperinsulinemia.

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Section: Discussionmentioning

confidence: 99%

Greater replication and differentiation of preadipocytes in inherited corticosteroid-binding globulin deficiency

Joyner

Hutley

Bachmann

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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“…There is evidence for extra-hepatic CBG synthesis in lung, ovary, endometrium, trophoblast cells, neonatal kidney and fetal exocrine pancreas and pituitary (Hammond et al 1987, Scrocchi et al 1993a,b, Berdusco et al 1995, Misao et al 1995, Seralini 1996, Benassayag et al 2001. In contrast to cellular internalization of the CBG-CORT complex, which serves to locally increase free CORT levels, cellular synthesis of CBG is thought to limit the accessibility of CORT to the intracellular receptors.…”

Section: Intracellular Localization Of Cbgmentioning

confidence: 99%

Plasma binding proteins as mediators of corticosteroid action in vertebrates

Breuner

Orchinik

2002

Journal of Endocrinology

414

244

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Stressors elicit a complex but variable suite of endocrine events. Comparative studies of the stress response have focused primarily on the adrenocortical response to stress, in particular the measurement of plasma levels of glucocorticoids. However, a number of other factors contribute to and modify cellular and organismal responses to glucocorticoids. Notably, plasma corticosteroid binding globulins (CBGs) can regulate the general availability of steroid to tissues, and/or direct the delivery of hormones to specific sites. In this paper, we discuss possible functions of CBG and mechanisms of CBG action, review CBG characteristics among vertebrates, and discuss our recent studies indicating that CBG may indeed modulate responses to stressors. For example, in house sparrows, we found that basal and stress-induced concentrations of total corticosteroid (cortisol or corticosterone) (CORT) vary seasonally, but CBG concentrations change proportionally, so that free CORT concentrations appear static yearround. In contrast, in white-crowned sparrows and tree lizards, CBG concentrations change under conditions when total CORT levels do not, resulting in significant changes in circulating free CORT. These differences in free CORT are masked if CBG is not accounted for. We have also found that the binding properties of CBG vary considerably between species and need to be determined empirically. Such studies led to the observation that CBG in several species may also serve as a functional androgen binding protein; this is especially important for birds, because previous studies had concluded that birds lack androgen binding globulins. We propose that consideration of CBG is paramount to understanding the role of glucocorticoids in mediating behavioral and physiological responses to stress.

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“…Female pups have higher circulating concentrations of CBG resulting in decreased corticosterone negative feedback upon immune and HPA function relative to male pups (McCormick et al 2002;Shanks et al 1994). In the human placenta, cortisol bioavailability is probably controlled by 11β-HSD 2 activity (Patel et al 1999) and possibly CBG (Dancis et al 1978;Misao et al 1999;Benassayag et al 2001). However, no sex-specific differences are known in placental CBG.…”

Section: Sex-specific Differences Of Fetal Immunitymentioning

confidence: 99%

Sexually dimorphic effects of maternal asthma during pregnancy on placental glucocorticoid metabolism and fetal growth

Clifton

2005

Cell Tissue Res

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Human pregnancy is associated with sexually dimorphic differences in mortality and morbidity of the fetus with the male fetus experiencing the poorest outcome following complications such as pre-eclampsia, pre-term delivery and infection. The physiological mechanisms that confer these differences have not been well characterised in the human. Work conducted on the effect of maternal asthma during pregnancy, combining data collected from the mother, placenta and fetus has found some significant sex-related mechanistic differences associated with fetal growth in both normal pregnancies and pregnancies complicated by asthma. Specifically, sexually dimorphic differences have been found in placental glucocorticoid metabolism in male and female fetuses of normal pregnancies. In response to the presence of maternal asthma, only the female fetus alters placental glucocorticoid metabolism resulting in decreased growth. The male fetus does not alter placental function or growth in response to maternal asthma. As a result of the alterations in glucocorticoid metabolism in the female, downstream changes occur in pathways regulated by glucocorticoids. These data suggest that the female fetus adjusts placental function and reduces growth to compensate for maternal disease. However, the male fetus continues to grow in response to maternal asthma with no changes in placental function. This response by the male fetus may partially contribute to the increased risk of morbidity and mortality in this sex.

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Corticosteroid-Binding Globulin Status at the Fetomaternal Interface During Human Term Pregnancy1

Cited by 37 publications

References 37 publications

Greater replication and differentiation of preadipocytes in inherited corticosteroid-binding globulin deficiency

Greater replication and differentiation of preadipocytes in inherited corticosteroid-binding globulin deficiency

Plasma binding proteins as mediators of corticosteroid action in vertebrates

Sexually dimorphic effects of maternal asthma during pregnancy on placental glucocorticoid metabolism and fetal growth

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