Adiponectin and leptin systems in human endometrium during window of implantation

Santos, Esther Dos; Sérazin, Valérie; Morvan, Corinne; Torre, Antoine; Wainer, R.; Mazancourt, Philippe de; Dieudonné, Marie‐Noëlle

doi:10.1016/j.fertnstert.2011.12.042

Cited by 65 publications

(62 citation statements)

References 56 publications

(59 reference statements)

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“…The deficiency of leptin or LEPR due to lossof-function mutations in the corresponding genes has been linked to infertility and delayed puberty development in humans and rodents. Moreover, leptin and its receptor have been implicated in maintaining other normal female reproductive functions, including lactation, folliculogenesis, ovarian steroidogenesis, the maintenance of mammary gland morphology and function, the development of dominant follicles and oocytes, maturation endometrial development, menstrual cycle regulation (Agarwal et al 1999, Zachow et al 1999, and endometrial receptivity (Marin Bivens & Olster 1997, Bluher & Mantzoros 2007, Israel & Chua 2010, Clempson et al 2011, Dos Santos et al 2012. Leptin signaling also contributes to the hypothalamic-pituitary-gonadal (HPG) axis.…”

Section: Leptinmentioning

confidence: 99%

Adipokines in reproductive function: a link between obesity and polycystic ovary syndrome

Chen¹,

Jia²,

Qiao³

et al. 2013

Journal of Molecular Endocrinology

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Polycystic ovary syndrome (PCOS) is the most common endocrinopathy associated with infertility and metabolic disorder in women of reproductive age. Dysfunction of adipose tissue has been implicated in the pathophysiology of PCOS. Increasing evidence shows that the dysregulated expression of adipokines, the secreted products of adipose tissue, plays an important role in the pathology of PCOS. Here, we review the role of several identified adipokines that may act as a link between obesity and PCOS. PCOS also reciprocally influences the profile of adipokines. Insight into the underlying mechanisms will help better understand the pathology of PCOS and identify new therapeutic targets of this syndrome.

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Section: Leptinmentioning

confidence: 99%

Adipokines in reproductive function: a link between obesity and polycystic ovary syndrome

Chen¹,

Jia²,

Qiao³

et al. 2013

Journal of Molecular Endocrinology

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“…A study showed that expression of ADIPOR1 and ADIPOR2 peaks in the mid-secretory phase of menstrual cycle (Takemura et al 2006). We have also observed significantly low endometrial expression of ADIPOR1 and ADIPOR2 in women with unexplained recurrent implantation failure relative to fertile women (Dos Santos et al 2012). In vitro, adiponectin exerts an anti-proliferative action by promoting cell death (Bohlouli et al 2013).…”

Section: Introductionmentioning

confidence: 62%

“…It is now established that adiponectin is not produced by human trophoblastic cells but seems to be expressed in human endometrium (Takemura et al 2006, Benaitreau et al 2010a, Dos Santos et al 2012. ADIPOR1 and ADIPOR2 are expressed in human placenta and endometrium (Takemura et al 2006, Benaitreau et al 2009.…”

Section: Introductionmentioning

confidence: 99%

Adiponectin limits differentiation and trophoblast invasion in human endometrial cells

Duval

Santos

Moindjie

et al. 2017

Journal of Molecular Endocrinology

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Successful human embryo implantation requires a proper differentiation of endometrial stromal cells (ESCs) into decidual cells, during a process called decidualization. ESCs express specific molecules, such as prolactin, insulin-like growth factor-binding protein-1 (IGFBP-1) and connexin-43. Decidual cells are also involved in the control of trophoblast invasion, by secreting various factors, such as matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). Adiponectin is an adipokine with insulin-sensitizing, anti-inflammatory and anti-proliferative effects. At the embryomaternal interface, adiponectin promotes differentiation and invasion of human trophoblastic cells. We hypothesize that the effects of adiponectin on endometrium could counteract its pro-invasive effects previously described in the human trophoblast. In this context, we have firstly demonstrated that adiponectin downregulates IGFBP-1 and connexin-43 mRNA expressions, as well as prolactin secretion in ESCs, suggesting an anti-differentiative effect of adiponectin. Secondly, we found that invasive capacities of trophoblastic cell line HTR-8/SVneo are reduced in the presence of conditioned media from ESC cultured in the presence of adiponectin. Adiponectin's anti-invasive action is associated with a decreased activity of MMP-2 and MMP-9, and an increased TIMP-3 mRNA expression in ESCs. Finally, adiponectin receptors (ADIPOR1 and ADIPOR2) knockdown abolishes the anti-differentiative and anti-invasive effects of adiponectin in human ESCs. Altogether, our results suggest that adiponectin reduces the decidualization process and inversely induces the production of endometrial factors that limit trophoblast invasion. Thus, through a dual control in trophoblast and endometrial cells, adiponectin appears as a pivotal actor of the embryo implantation process.

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“…Chez la femme, une forte expression des récepteurs a été observée dans l'endomètre pendant la période de l'implantation de l'embryon. Une étude récente indique que l'expression d'AdipoR1 et AdipoR2 est diminuée (60 %) dans l'endomètre des femmes en échec d'implantation après une procédure de FIV (fécondation in vitro) pour infertilité comparée à l'expression dans l'endomètre de femmes fertiles [38]. D'autre part, les taux plasmatiques d'adiponectine sont fortement diminués chez des patientes atteintes de diabète gestationnel, du syndrome des ovaires polykystiques (SOPK), mais aussi d'endométriose et de cancer de l'endomètre (voir [18]).…”

Section: Rôle De L'adiponectine Et De La Résistine Au Cours De L'implunclassified

“…D'autre part, les taux plasmatiques d'adiponectine sont fortement diminués chez des patientes atteintes de diabète gestationnel, du syndrome des ovaires polykystiques (SOPK), mais aussi d'endométriose et de cancer de l'endomètre (voir [18]). Ces études suggèrent qu'une modification de l'expression de l'adiponectine et/ou de ses récepteurs pourrait être impliquée dans la réceptivité endométriale [38,39]. De plus, une dérégulation de l'expression de ce système pourrait survenir dans certaines conditions pathologiques associées à des fausses couches ou à des pathologies de l'implantation [39].…”

Section: Rôle De L'adiponectine Et De La Résistine Au Cours De L'implunclassified

Adiponectine et résistine

et al. 2013

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Adiponectin and leptin systems in human endometrium during window of implantation

Cited by 65 publications

References 56 publications

Adipokines in reproductive function: a link between obesity and polycystic ovary syndrome

Adipokines in reproductive function: a link between obesity and polycystic ovary syndrome

Adiponectin limits differentiation and trophoblast invasion in human endometrial cells

Adiponectine et résistine

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