In vitro steroidogenic effects of neuropeptide Y (NPY1–36), Y1 and Y2 receptor agonists (Leu31-Pro34 NPY, NPY18–36) and peptide YY (PYY) on rat adrenal capsule/zona glomerulosa

Bernet, François; Maubert, Eric; Bernard, Jacqueline; Montel, Valérie; Dupouy, Jean‐Paul

doi:10.1016/0167-0115(94)90053-1

Cited by 32 publications

(18 citation statements)

References 16 publications

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“…Corticosterone and estradiol concentrations in plasma were measured by radio-immuno assay as previously described (Bernet et al, 1994;Lesage et al, 1996, respectively). Quantitative determination of progesterone in the plasma has been performed by a radio-immuno assay kit (PROG-CTRIA) purchased from Cis Bio International (Gif-surYvette, France).…”

Section: Quantitative Determination Of Circulating Hormonesmentioning

confidence: 99%

Steroid hormones modulate H19 gene expression in both mammary gland and uterus

et al. 1999

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H19 is an imprinted and developmentally regulated gene whose product remains apparently untranslated. In a previous study on breast adenocarcinomas, we reported that overexpression of the H19 gene was signi®cantly correlated with the presence of steroid receptors, suggesting the putative role of hormones in H19 transcription. To determine the mode of steroid action, we have detected levels of H19 RNA synthesis during mammary gland development by in situ hybridization (ISH): two peaks of H19 transcription occur during puberty and pregnancy. Furthermore, we demonstrated by ISH that in the uterus H19 RNA synthesis is high during estrus and metestrus phases. To test steroid control of H19 transcription, ovariectomized and adrenalectomized mice were supplemented, 1 week after surgery, with 17-b-estradiol (E2, 20 mg/kg/day), progesterone (P, 1 mg/kg/day) or corticosterone (B, 0.3 mg/ kg/day) for 2 weeks. According to ISH data, E2 and to a lesser extent B stimulated H19 transcription in the uterus, whereas P inhibited it. To con®rm the in vivo results, in vitro experiments were performed using cultures of MCF-7 cells (a hormone-sensitive mammary cell line). E2 stimulated the endogenous H19 gene of this cell line and tamoxifen inhibited this e ect. Furthermore, we performed transient cotransfections in MCF-7, in HBL-100 (another hormone-sensitive mammary cell line) and in BT-20 (a hormone-insensitive mammary cell line) with various constructs of ERa (WT or mutated) and PR-A, in presence or absence of steroid hormones. We demonstrated that ERa up-regulated the H19 promoter in MCF-7 and in HBL-100, whereas PR-A did not have any e ect per se. Moreover, in MCF-7, PR-A antagonized clearly the ERa-mediated promoter enhancement, but in HBL-100 this counteracting e ect on the ERa up-regulation was not found. Interestingly, the same experiments performed in BT-20 cell line provided very similar results as those obtained in MCF-7 cells, with a clear down-regulation mediated by PR-A on the H19 promoter. All these in vitro data are in agreement with in vivo results. In addition, data obtained with ERa mutants indicate that H19 promoter activation is both ligand-dependent and ligand-independent. We have thus demonstrated that H19 gene expression is controlled by steroid hormones; furthermore, this gene is highly expressed in hormone-sensitive organs when the hormonal stimulation is accompanied with a morphological repair.

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Section: Quantitative Determination Of Circulating Hormonesmentioning

confidence: 99%

Steroid hormones modulate H19 gene expression in both mammary gland and uterus

et al. 1999

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“…Insulin levels in plasma were determined by the Ultrasensitive rat insulin ELISA and the pancreatic insulin content using the high range rat insulin ELISA (Mercodia, Uppsala, Sweden). Corticosterone levels were determined using an RIA with highly specific corticosterone antiserum (UCB Bioproducts, Paris, France), as previously described [19].…”

Section: Methodsmentioning

confidence: 99%

Different mechanisms operating during different critical time-windows reduce rat fetal beta cell mass due to a maternal low-protein or low-energy diet

et al. 2007

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Aims/hypothesis Adverse events during intra-uterine life may programme organ growth and favour disease later in life. In animals, protein or energy restriction during gestation alters the development of the endocrine pancreas, even though the duration of malnutrition is different. Here, we evaluate the specific effects of both diets during different periods of gestation and the mechanisms underlying the decreased beta cell mass. Methods Pregnant Wistar rats were fed either a low-protein or a low-energy diet during the last week of gestation or throughout gestation. Fetuses and their pancreases were analysed at days 15 and 21 of gestation. Results The low-energy diet reduced the beta cell mass from 21-day-old fetuses by 33 or 56% when administered during the last week or throughout gestation, respectively. Fetal corticosterone levels were increased. At 15 days of fetal age, the number of cells producing neurogenin 3 (NEUROG3) or pancreatic and duodenal homeobox gene 1 (PDX-1) was reduced. Neither islet vascularisation nor beta cell proliferation was affected. The low-protein diet, in contrast, was more efficient in decreasing the fetal beta cell mass when given during the last week of gestation (−53%) rather than throughout gestation (−33%). Beta cell proliferation was decreased by 50% by the low-protein diet, independently of its duration, and islet vascularisation was reduced. This diet did not affect NEUROG3-or PDX-1-positive cell numbers. Conclusion/interpretation Although both diets reduced the fetal beta cell mass, the cellular mechanisms and the sensitivity windows were different. Early alteration of neogenesis due to elevated corticosterone levels is likely to be responsible for the decreased beta cell mass in low-energy fetuses, whereas impaired beta cell proliferation and islet vascularisation at later stages are implicated in low-protein fetuses. Keywords

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“…Acute administration of NPY to rats increases the concentrations of circulating aldosterone (24) and enhances the release of aldosterone in adrenals perfused in situ (25) and through isolated specimens of the adrenal capsule and ZG (26). Chronic administration of NPY to rats with damaged HPA axis and renin-angiotensin system (RAS) stimulates ZG to grow and to synthesize steroids (27).…”

Section: Role Of Npy In Regulation Of the Hpa Axis In Adrenal Glandsmentioning

confidence: 99%

“…In addition, results from studies of dogs and rats are inconsistent. It has been shown that only intact NPY can stimulate ACTH and cortisol release in dogs, whereas its C-terminal fragment, NPY (19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36), and the NPY analog, NPY (1-36)-OH, are ineffective (12). In contrast, Small et al (18), using different NPY analogs, have obtained results suggesting that the rat hypothalamic NPY receptor, which increased plasma ACTH concentrations, has a fragment activation profile unlike those of Y1-Y4 and Y6 receptors, and appears distinct from the NPY receptor controlling food intake.…”

Section: Role Of Npy In Regulation Of the Hpa Axis In The Hypothalamusmentioning

confidence: 99%

Interactions between the neuropeptide Y system and the hypothalamic-pituitary-adrenal axis

Krysiak¹,

Obuchowicz²,

Herman³

1999

European Journal of Endocrinology

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The aim of this paper is to review the present knowledge of interactions between the neuropeptide Y (NPY) system and the hypothalamic-pituitary-adrenal (HPA) axis. On the basis of in vitro and in vivo studies of various animal species, we review the effects of NPY on all levels of HPA axis activity. We also describe the effects of glucocorticosteroids on the NPY system in the hypothalamus, including interactions between glucocorticosteroids and insulin. On the basis of available literature, we discuss the role of these interactions in the control of food intake and in the pathogenesis of obesity.

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In vitro steroidogenic effects of neuropeptide Y (NPY1–36), Y1 and Y2 receptor agonists (Leu31-Pro34 NPY, NPY18–36) and peptide YY (PYY) on rat adrenal capsule/zona glomerulosa

Cited by 32 publications

References 16 publications

Steroid hormones modulate H19 gene expression in both mammary gland and uterus

Steroid hormones modulate H19 gene expression in both mammary gland and uterus

Different mechanisms operating during different critical time-windows reduce rat fetal beta cell mass due to a maternal low-protein or low-energy diet

Interactions between the neuropeptide Y system and the hypothalamic-pituitary-adrenal axis

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