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  1. Book ; Online: Endocrine Disrupters and Metabolism

    Gibert, Yann / Nadal, Angel / Sargis, Robert

    2020  

    Keywords Medicine ; Endocrinology ; endocrine disrupters ; metabolism ; metabolic diseases ; lipids ; diabetes ; pancreas ; adipose tissue
    Size 1 electronic resource (259 pages)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021230122
    ISBN 9782889634224 ; 2889634221
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: The Commonly Overlooked Factor. Commentary on: "Environmental Obesogens and their Impact on Susceptibility to Obesity".

    Alonso-Magdalena, Paloma / Nadal, Angel

    Endocrinology

    2020  Volume 161, Issue 9

    MeSH term(s) Animals ; Dietary Supplements ; Kisspeptins ; Male ; Mice ; Mice, Knockout ; Obesity ; Spermatogenesis ; Spermatozoa ; Testosterone
    Chemical Substances Kiss1 protein, mouse ; Kisspeptins ; Testosterone (3XMK78S47O)
    Language English
    Publishing date 2020-10-11
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 427856-2
    ISSN 1945-7170 ; 0013-7227
    ISSN (online) 1945-7170
    ISSN 0013-7227
    DOI 10.1210/endocr/bqaa123
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Deucravacitinib, a tyrosine kinase 2 pseudokinase inhibitor, protects human EndoC-βH1 β-cells against proinflammatory insults.

    Dos Santos, Reinaldo S / Guzman-Llorens, Daniel / Perez-Serna, Atenea A / Nadal, Angel / Marroqui, Laura

    Frontiers in immunology

    2023  Volume 14, Page(s) 1263926

    Abstract: Introduction: Type 1 diabetes is characterized by pancreatic islet inflammation and autoimmune-driven pancreatic β-cell destruction. Interferon-α (IFNα) is a key player in early human type 1 diabetes pathogenesis. IFNα activates the tyrosine kinase 2 ( ... ...

    Abstract Introduction: Type 1 diabetes is characterized by pancreatic islet inflammation and autoimmune-driven pancreatic β-cell destruction. Interferon-α (IFNα) is a key player in early human type 1 diabetes pathogenesis. IFNα activates the tyrosine kinase 2 (TYK2)-signal transducer and activator of transcription (STAT) pathway, leading to inflammation, HLA class I overexpression, endoplasmic reticulum (ER) stress, and β-cell apoptosis (in synergy with IL-1β). As TYK2 inhibition has raised as a potential therapeutic target for the prevention or treatment of type 1 diabetes, we investigated whether the selective TYK2 inhibitor deucravacitinib could protect β-cells from the effects of IFNα and other proinflammatory cytokines (i.e., IFNγ and IL-1β).
    Methods: All experiments were performed in the human EndoC-βH1 β-cell line. HLA class I expression, inflammation, and ER stress were evaluated by real-time PCR, immunoblotting, and/or immunofluorescence. Apoptosis was assessed by the DNA-binding dyes Hoechst 33342 and propidium iodide or caspase 3/7 activity. The promoter activity was assessed by luciferase assay.
    Results: Deucravacitinib prevented IFNα effects, such as STAT1 and STAT2 activation and MHC class I hyperexpression, in a dose-dependent manner without affecting β-cell survival and function. A comparison between deucravacitinib and two Janus kinase inhibitors, ruxolitinib and baricitinib, showed that deucravacitinib blocked IFNα- but not IFNγ-induced signaling pathway. Deucravacitinib protected β-cells from the effects of two different combinations of cytokines: IFNα + IL-1β and IFNγ + IL-1β. Moreover, this TYK2 inhibitor could partially reduce apoptosis and inflammation in cells pre-treated with IFNα + IL-1β or IFNγ + IL-1β.
    Discussion: Our findings suggest that, by protecting β-cells against the deleterious effects of proinflammatory cytokines without affecting β-cell function and survival, deucravacitinib could be repurposed for the prevention or treatment of early type 1 diabetes.
    MeSH term(s) Humans ; TYK2 Kinase ; Diabetes Mellitus, Type 1/metabolism ; Cytokines/pharmacology ; Interferon-alpha/metabolism ; Inflammation
    Chemical Substances TYK2 Kinase (EC 2.7.10.2) ; deucravacitinib (N0A21N6RAU) ; Cytokines ; Interferon-alpha
    Language English
    Publishing date 2023-10-03
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1263926
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Obesity: Fat from plastics? Linking bisphenol A exposure and obesity.

    Nadal, Angel

    Nature reviews. Endocrinology

    2012  Volume 9, Issue 1, Page(s) 9–10

    MeSH term(s) Benzhydryl Compounds/adverse effects ; Benzhydryl Compounds/urine ; Humans ; Obesity/urine ; Phenols/adverse effects ; Phenols/urine ; Plastics/adverse effects
    Chemical Substances Benzhydryl Compounds ; Phenols ; Plastics ; bisphenol A (MLT3645I99)
    Language English
    Publishing date 2012-11-13
    Publishing country England
    Document type News
    ZDB-ID 2489381-X
    ISSN 1759-5037 ; 1759-5029
    ISSN (online) 1759-5037
    ISSN 1759-5029
    DOI 10.1038/nrendo.2012.205
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  5. Article ; Online: In Vitro Assays to Identify Metabolism-Disrupting Chemicals with Diabetogenic Activity in a Human Pancreatic β-Cell Model.

    Dos Santos, Reinaldo Sousa / Medina-Gali, Regla María / Babiloni-Chust, Ignacio / Marroqui, Laura / Nadal, Angel

    International journal of molecular sciences

    2022  Volume 23, Issue 9

    Abstract: There is a need to develop identification tests for Metabolism Disrupting Chemicals (MDCs) with diabetogenic activity. Here we used the human EndoC-βH1 β-cell line, the rat β-cell line INS-1E and dispersed mouse islet cells to assess the effects of ... ...

    Abstract There is a need to develop identification tests for Metabolism Disrupting Chemicals (MDCs) with diabetogenic activity. Here we used the human EndoC-βH1 β-cell line, the rat β-cell line INS-1E and dispersed mouse islet cells to assess the effects of endocrine disruptors on cell viability and glucose-stimulated insulin secretion (GSIS). We tested six chemicals at concentrations within human exposure (from 0.1 pM to 1 µM). Bisphenol-A (BPA) and tributyltin (TBT) were used as controls while four other chemicals, namely perfluorooctanoic acid (PFOA), triphenylphosphate (TPP), triclosan (TCS) and dichlorodiphenyldichloroethylene (DDE), were used as "unknowns". Regarding cell viability, BPA and TBT increased cell death as previously observed. Their mode of action involved the activation of estrogen receptors and PPARγ, respectively. ROS production was a consistent key event in BPA-and TBT-treated cells. None of the other MDCs tested modified viability or ROS production. Concerning GSIS, TBT increased insulin secretion while BPA produced no effects. PFOA decreased GSIS, suggesting that this chemical could be a "new" diabetogenic agent. Our results indicate that the EndoC-βH1 cell line is a suitable human β-cell model for testing diabetogenic MDCs. Optimization of the test methods proposed here could be incorporated into a set of protocols for the identification of MDCs.
    MeSH term(s) Animals ; Benzhydryl Compounds/metabolism ; Benzhydryl Compounds/toxicity ; Endocrine Disruptors/metabolism ; Endocrine Disruptors/toxicity ; Glucose/metabolism ; Humans ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Mice ; Rats ; Reactive Oxygen Species/metabolism
    Chemical Substances Benzhydryl Compounds ; Endocrine Disruptors ; Reactive Oxygen Species ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2022-05-01
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23095040
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Rapid responses to steroid hormones. Preface.

    Nadal, Angel

    Steroids

    2010  Volume 75, Issue 8-9, Page(s) 519

    MeSH term(s) Hormones/metabolism ; Humans ; Signal Transduction ; Steroids/metabolism
    Chemical Substances Hormones ; Steroids
    Language English
    Publishing date 2010-08
    Publishing country United States
    Document type Introductory Journal Article
    ZDB-ID 80312-1
    ISSN 1878-5867 ; 0039-128X
    ISSN (online) 1878-5867
    ISSN 0039-128X
    DOI 10.1016/j.steroids.2010.02.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 87: Show issues Location:
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  7. Article ; Online: BCL-XL Overexpression Protects Pancreatic β-Cells against Cytokine- and Palmitate-Induced Apoptosis.

    Perez-Serna, Atenea A / Dos Santos, Reinaldo S / Ripoll, Cristina / Nadal, Angel / Eizirik, Decio L / Marroqui, Laura

    International journal of molecular sciences

    2023  Volume 24, Issue 6

    Abstract: Diabetes is a chronic disease that affects glucose metabolism, either by autoimmune-driven β-cell loss or by the progressive loss of β-cell function, due to continued metabolic stresses. Although both α- and β-cells are exposed to the same stressors, ... ...

    Abstract Diabetes is a chronic disease that affects glucose metabolism, either by autoimmune-driven β-cell loss or by the progressive loss of β-cell function, due to continued metabolic stresses. Although both α- and β-cells are exposed to the same stressors, such as proinflammatory cytokines and saturated free fatty acids (e.g., palmitate), only α-cells survive. We previously reported that the abundant expression of BCL-XL, an anti-apoptotic member of the BCL-2 family of proteins, is part of the α-cell defense mechanism against palmitate-induced cell death. Here, we investigated whether BCL-XL overexpression could protect β-cells against the apoptosis induced by proinflammatory and metabolic insults. For this purpose, BCL-XL was overexpressed in two β-cell lines-namely, rat insulinoma-derived INS-1E and human insulin-producing EndoC-βH1 cells-using adenoviral vectors. We observed that the BCL-XL overexpression in INS-1E cells was slightly reduced in intracellular Ca
    MeSH term(s) Animals ; Humans ; Rats ; Apoptosis/genetics ; Cell Line ; Cytokines/metabolism ; Insulin-Secreting Cells/metabolism ; Palmitates/pharmacology ; Palmitates/metabolism
    Chemical Substances Cytokines ; Palmitates ; BCL2L1 protein, human ; Bcl2l1 protein, rat
    Language English
    Publishing date 2023-03-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24065657
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Endocrine disruptors in plastics alter β-cell physiology and increase the risk of diabetes mellitus.

    Martínez-Pinna, Juan / Sempere-Navarro, Roberto / Medina-Gali, Regla M / Fuentes, Esther / Quesada, Ivan / Sargis, Robert M / Trasande, Leonardo / Nadal, Angel

    American journal of physiology. Endocrinology and metabolism

    2023  Volume 324, Issue 6, Page(s) E488–E505

    Abstract: Plastic pollution breaks a planetary boundary threatening wildlife and humans through its physical and chemical effects. Of the latter, the release of endocrine disrupting chemicals (EDCs) has consequences on the prevalence of human diseases related to ... ...

    Abstract Plastic pollution breaks a planetary boundary threatening wildlife and humans through its physical and chemical effects. Of the latter, the release of endocrine disrupting chemicals (EDCs) has consequences on the prevalence of human diseases related to the endocrine system. Bisphenols (BPs) and phthalates are two groups of EDCs commonly found in plastics that migrate into the environment and make low-dose human exposure ubiquitous. Here we review epidemiological, animal, and cellular studies linking exposure to BPs and phthalates to altered glucose regulation, with emphasis on the role of pancreatic β-cells. Epidemiological studies indicate that exposure to BPs and phthalates is associated with diabetes mellitus. Studies in animal models indicate that treatment with doses within the range of human exposure decreases insulin sensitivity and glucose tolerance, induces dyslipidemia, and modifies functional β-cell mass and serum levels of insulin, leptin, and adiponectin. These studies reveal that disruption of β-cell physiology by EDCs plays a key role in impairing glucose homeostasis by altering the mechanisms used by β-cells to adapt to metabolic stress such as chronic nutrient excess. Studies at the cellular level demonstrate that BPs and phthalates modify the same biochemical pathways involved in adaptation to chronic excess fuel. These include changes in insulin biosynthesis and secretion, electrical activity, expression of key genes, and mitochondrial function. The data summarized here indicate that BPs and phthalates are important risk factors for diabetes mellitus and support a global effort to decrease plastic pollution and human exposure to EDCs.
    MeSH term(s) Animals ; Humans ; Endocrine Disruptors ; Diabetes Mellitus ; Insulin ; Cell Physiological Phenomena ; Glucose
    Chemical Substances Endocrine Disruptors ; Insulin ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2023-05-03
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 603841-4
    ISSN 1522-1555 ; 0193-1849
    ISSN (online) 1522-1555
    ISSN 0193-1849
    DOI 10.1152/ajpendo.00068.2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uc I Zs.89: Show issues Location:
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  9. Book ; Conference proceedings: The Sixth International Meeting on Rapid Responses to Steroid Hormones, RRSH2009, Elche, Spain

    Nadal, Ángel

    (Steroids : Special issue ; 75.2010,8/9)

    2010  

    Institution International Meeting on Rapid Responses to Steroid Hormones
    Event/congress International Meeting on Rapid Responses to Steroid Hormones (6, 2009.09.02-05, Elche) ; RRSH (6, 2009.09.02-05, Elche)
    Author's details guest ed. Ángel Nadal
    Series title Steroids : Special issue ; 75.2010,8/9
    Language English
    Size VI S., S. 519 - 623, Ill., graph. Darst.
    Publisher Elsevier
    Publishing place Amsterdam u.a.
    Document type Book ; Conference proceedings
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  10. Article: Editorial: Endocrine Disrupters and Metabolism.

    Gibert, Yann / Sargis, Robert M / Nadal, Angel

    Frontiers in endocrinology

    2019  Volume 10, Page(s) 859

    Language English
    Publishing date 2019-12-10
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2019.00859
    Database MEDical Literature Analysis and Retrieval System OnLINE

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