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248 results on '"Alonso-Magdalena, Paloma"'

14. Combinatorial pathway disruption is a powerful approach to delineate metabolic impacts of endocrine disruptors

Author

Bernal, Kévin, primary, Touma, Charbel, additional, Erradhouani, Chedi, additional, Boronat‐Belda, Talía, additional, Gaillard, Lucas, additional, Al Kassir, Sara, additional, Le Mentec, Hélène, additional, Martin‐Chouly, Corinne, additional, Podechard, Normand, additional, Lagadic‐Gossmann, Dominique, additional, Langouet, Sophie, additional, Brion, François, additional, Knoll‐Gellida, Anja, additional, Babin, Patrick J., additional, Sovadinova, Iva, additional, Babica, Pavel, additional, Andreau, Karine, additional, Barouki, Robert, additional, Vondracek, Jan, additional, Alonso‐Magdalena, Paloma, additional, Blanc, Etienne, additional, Kim, Min Ji, additional, and Coumoul, Xavier, additional

Published
2022
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24. Integrative strategy of testing systems for identification of endocrine disruptors inducing metabolic disorders-an introduction to the OBERON project

Author

Audouze, Karine, Sarigiannis, Denis, Alonso-Magdalena, Paloma, Brochot, Céline, Casas, Maribel, Vrijheid, Martine, Babin, Patrick J., Karakitsios, Spryros, Coumoul, Xavier, Barouki, Robert, Toxicité environnementale, cibles thérapeutiques, signalisation cellulaire (T3S - UMR_S 1124), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Aristotle University of Thessaloniki, Universidad Miguel Hernández [Elche] (UMH), Institut National de l'Environnement Industriel et des Risques (INERIS), Instituto de Salud Global - Institute For Global Health [Barcelona] (ISGlobal), Universitat Pompeu Fabra [Barcelona] (UPF), CIBER de Epidemiología y Salud Pública (CIBERESP), Laboratoire Maladies Rares: Génétique et Métabolisme (Bordeaux) (U1211 INSERM/MRGM), Université de Bordeaux (UB)-Groupe hospitalier Pellegrin-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Civs, Gestionnaire, and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)

Subjects
Project Report, Adverse outcome pathways, obesity, non-animal testing, Metabolic disorders, Regional Medical Programs, Risk Assessment, lcsh:Chemistry, Metabolic Diseases, Integrative approach, Predictive toxicology, [SDV.EE.SANT] Life Sciences [q-bio]/Ecology, environment/Health, Animals, Humans, Non-animal testing, lcsh:QH301-705.5, Endocrine disruptors, Non-alcoholic fatty liver diseases, [SDV.EE.SANT]Life Sciences [q-bio]/Ecology, environment/Health, Systems Biology, Computational systems toxicology, Computational Biology, [SDV.TOX] Life Sciences [q-bio]/Toxicology, Europe, Metabolism, lcsh:Biology (General), lcsh:QD1-999, [SDV.TOX]Life Sciences [q-bio]/Toxicology, Biological Assay, Disease Susceptibility, Biomarkers
Abstract

Exposure to chemical substances that can produce endocrine disrupting effects represents one of the most critical public health threats nowadays. In line with the regulatory framework implemented within the European Union (EU) to reduce the levels of endocrine disruptors (EDs) for consumers, new and effective methods for ED testing are needed. The OBERON project will build an integrated testing strategy (ITS) to detect ED-related metabolic disorders by developing, improving and validating a battery of test systems. It will be based on the concept of an integrated approach for testing and assessment (IATA). OBERON will combine (1) experimental methods (in vitro, e.g., using 2D and 3D human-derived cells and tissues, and in vivo, i.e., using zebrafish at different stages), (2) high throughput omics technologies, (3) epidemiology and human biomonitoring studies and (4) advanced computational models (in silico and systems biology) on functional endpoints related to metabolism. Such interdisciplinary framework will help in deciphering EDs based on a mechanistic understanding of toxicity by providing and making available more effective alternative test methods relevant for human health that are in line with regulatory needs. Data generated in OBERON will also allow the development of novel adverse outcome pathways (AOPs). The assays will be pre-validated in order to select the test systems that will show acceptable performance in terms of relevance for the second step of the validation process, i.e., the inter-laboratory validation as ring tests. Therefore, the aim of the OBERON project is to support the organization for economic co-operation and development (OECD) conceptual framework for testing and assessment of single and/or mixture of EDs by developing specific assays not covered by the current tests, and to propose an IATA for ED-related metabolic disorder detection, which will be submitted to the Joint Research Center (JRC) and OECD community. The authors would like to acknowledge OBERON (https://oberon-4eu.com/, a project funded by the European Union’s Horizon 2020 research and innovation program under grant agreement no. 825712.

Published
2020

27. Low doses of bisphenol A and diethylstilbestrol impair [Ca.sup.2+] signals in pancreatic [alpha]-cells through a nonclassical membrane estrogen receptor within intact islets of Langerhans

Author

Alonso-Magdalena, Paloma, Laribi, Ouahiba, Ropero, Ana B., Fuentes, Esther, Ripoll, Cristina, Soria, Bernat, and Nadal, Angel

Abstract

Glucagon, secreted from pancreatic [alpha]-cells integrated within the islets of Langerhans, is involved in the regulation of glucose metabolism by enhancing the synthesis and mobilization of glucose in the liver. [...]

Published
2005

30. The Effects of Aging on Male Mouse Pancreatic β-Cell Function Involve Multiple Events in the Regulation of Secretion: Influence of Insulin Sensitivity.

Author

Tudurí, Eva, Soriano, Sergi, Almagro, Lucía, García-Heredia, Anabel, Rafacho, Alex, Alonso-Magdalena, Paloma, Nadal, Ángel, and Quesada, Ivan

Subjects
INSULIN sensitivity, SECRETION, NAD (Coenzyme), TYPE 2 diabetes, AGING, ISLANDS of Langerhans, RESEARCH, ANIMAL experimentation, RESEARCH methodology, EVALUATION research, INSULIN, COMPARATIVE studies, GLUCOSE, CALCIUM, INSULIN resistance, MICE
Abstract

Aging is associated with a decline in peripheral insulin sensitivity and an increased risk of impaired glucose tolerance and type 2 diabetes. During conditions of reduced insulin sensitivity, pancreatic β cells undergo adaptive responses to increase insulin secretion and maintain euglycemia. However, the existence and nature of β-cell adaptations and/or alterations during aging are still a matter of debate. In this study, we investigated the effects of aging on β-cell function from control (3-month-old) and aged (20-month-old) mice. Aged animals were further categorized into 2 groups: high insulin sensitive (aged-HIS) and low insulin sensitive (aged-LIS). Aged-LIS mice were hyperinsulinemic, glucose intolerant, and displayed impaired glucose-stimulated insulin and C-peptide secretion, whereas aged-HIS animals showed characteristics in glucose homeostasis similar to controls. In isolated β cells, we observed that glucose-induced inhibition of KATP channel activity was reduced with aging, particularly in the aged-LIS group. Glucose-induced islet NAD(P)H production was decreased in aged mice, suggesting impaired mitochondrial function. In contrast, voltage-gated Ca2+ currents were higher in aged-LIS β cells, and pancreatic islets of both aged groups displayed increased glucose-induced Ca2+ signaling and augmented insulin secretion compared with controls. Morphological analysis of pancreas sections also revealed augmented β-cell mass with aging, especially in the aged-LIS group, as well as ultrastructural β-cell changes. Altogether, these findings indicate that aged mouse β cells compensate for the aging-induced alterations in the stimulus-secretion coupling, particularly by adjusting their Ca2+ influx to ensure insulin secretion. These results also suggest that decreased peripheral insulin sensitivity exacerbates the effects of aging on β cells. [ABSTRACT FROM AUTHOR]

Published
2022
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40. Pancreatic alpha-cell mass in the early-onset and advanced stage of a mouse model of experimental autoimmune diabetes

Author

Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), European Commission, Bru-Tarí, Eva, Cobo-Vuilleumier, Nadia, Alonso-Magdalena, Paloma, Dos Santos, Reinaldo S., Marroqui, Laura, Nadal, Ángel, Gauthier, Benoit R., Quesada, Iván, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), European Commission, Bru-Tarí, Eva, Cobo-Vuilleumier, Nadia, Alonso-Magdalena, Paloma, Dos Santos, Reinaldo S., Marroqui, Laura, Nadal, Ángel, Gauthier, Benoit R., and Quesada, Iván

Abstract

Most studies in type 1 diabetes (T1D) have focused on the loss of the pancreatic beta-cell population. However, despite the involvement of the alpha-cell in the aetiology and complications of T1D, little is known about the regulation of the pancreatic alpha-cell mass in this disease. The need for a better understanding of this process is further emphasized by recent findings suggesting that alpha-cells may constitute a potential reservoir for beta-cell regeneration. In this study, we characterized the pancreatic alpha-cell mass and its regulatory processes in the transgenic RIP-B7.1 mice model of experimental autoimmune diabetes (EAD). Diabetic mice presented insulitis, hyperglycaemia, hypoinsulinemia and hyperglucagonemia along with lower pancreatic insulin content. While alpha-cell mass and pancreatic glucagon content were preserved at the early-onset of EAD, both parameters were reduced in the advanced phase. At both stages, alpha-cell size, proliferation and ductal neogenesis were up-regulated, whereas apoptosis was almost negligible. Interestingly, we found an increase in the proportion of glucagon-containing cells positive for insulin or the beta-cell transcription factor PDX1. Our findings suggest that pancreatic alpha-cell renewal mechanisms are boosted during the natural course of EAD, possibly as an attempt to maintain the alpha-cell population and/or to increase beta-cell regeneration via alpha-cell transdifferentiation.

Published
2019

42. OR23-3 Differential Effects of Chronic Exposure to Bisphenol-A on Ion Channel Activity and Expression in Mouse Pancreatic Beta-Cells

Author

Nadal, Angel, primary, Marroqui, Laura, additional, Hmadcha, Abdelkrim, additional, Lopez-Beas, Javier, additional, Soriano, Sergi, additional, Villar-Pazos, Sabrina, additional, Alonso-Magdalena, Paloma, additional, Sousa dos Santos, Reinaldo, additional, Quesada, Ivan, additional, Fuentes, Esther, additional, Martin, Franz, additional, Soria, Bernat, additional, Gustafsson, Jan-Ake, additional, and Martinez-Pinna, Juan, additional

Published
2019
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43. Cortistatin regulates glucose-induced electrical activity and insulin secretion in mouse pancreatic beta-cells

Author

Soriano, Sergi, primary, Castellano-Muñoz, Manuel, additional, Rafacho, Alex, additional, Alonso-Magdalena, Paloma, additional, Marroquí, Laura, additional, Ruiz-Pino, Antonia, additional, Bru-Tarí, Eva, additional, Merino, Beatriz, additional, Irles, Esperanza, additional, Bello-Pérez, Melisa, additional, Iborra, Pau, additional, Villar-Pazos, Sabrina, additional, Vettorazzi, Jean F., additional, Montanya, Eduard, additional, Luque, Raúl M., additional, Nadal, Ángel, additional, and Quesada, Iván, additional

Published
2019
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46. Cortistatin regulates glucose-induced electrical activity and insulin secretion in mouse pancreatic beta-cells

Author

Universidad de Alicante. Departamento de Fisiología, Genética y Microbiología, Soriano, Sergi, Castellano-Muñoz, Manuel, Rafacho, Alex, Alonso Magdalena, Paloma, Marroquí, Laura, Ruiz, Antonia, Bru-Tarí, Eva, Merino, Beatriz, Irles, Esperanza, Bello, Melisa, Iborra, Pau, Villar-Pazos, Sabrina, Vettorazzi, Jean Franciesco, Montanya, Eduard, Luque, Raúl M., Nadal, Ángel, Quesada, Iván, Universidad de Alicante. Departamento de Fisiología, Genética y Microbiología, Soriano, Sergi, Castellano-Muñoz, Manuel, Rafacho, Alex, Alonso Magdalena, Paloma, Marroquí, Laura, Ruiz, Antonia, Bru-Tarí, Eva, Merino, Beatriz, Irles, Esperanza, Bello, Melisa, Iborra, Pau, Villar-Pazos, Sabrina, Vettorazzi, Jean Franciesco, Montanya, Eduard, Luque, Raúl M., Nadal, Ángel, and Quesada, Iván

Abstract

Although there is growing evidence that cortistatin regulates several functions in different tissues, its role in the endocrine pancreas is not totally known. Here, we aim to study the effect of cortistatin on pancreatic beta-cells and glucose-stimulated insulin secretion (GSIS). Exposure of isolated mouse islets to cortistatin inhibited GSIS. This effect was prevented using a somatostatin receptor antagonist. Additionally, cortistatin hyperpolarized the membrane potential and reduced glucose-induced action potentials in isolated pancreatic beta-cells. Cortistatin did not modify ATP-dependent K+ (KATP) channel activity. In contrast, cortistatin increased the activity of a small conductance channel with characteristics of G protein-coupled inwardly rectifying K+ (GIRK) channels. The cortistatin effects on membrane potential and GSIS were largely reduced in the presence of a GIRK channel antagonist and by down-regulation of GIRK2 with small interfering RNA. Thus, cortistatin acts as an inhibitory signal for glucose-induced electrical activity and insulin secretion in the mouse pancreatic beta-cell.

Published
2018

49. Maternal Exposure to Bisphenol-A During Pregnancy Increases Pancreatic β-Cell Growth During Early Life in Male Mice Offspring

Author

Alonso Magdalena, Paloma, García Arévalo, Marta, and Departamentos de la UMH::Biología Aplicada

Subjects
endocrine system, bisphenol-A, urogenital system, 577 - Bioquímica. Biología molecular. Biofísica [CDU], β-cells, Endocrine disruptors
Abstract

Alterations during development of metabolic key organs such as the endocrine pancreas affect the phenotype later in life. There is evidence that in utero or perinatal exposure to bisphenol-A (BPA) leads to impaired glucose metabolism during adulthood. However, how BPA exposure during pregnancy affects pancreatic β-cell growth and function in offspring during early life has not been explored. We exposed pregnant mice to either vehicle (control) or BPA (10 and 100 μg/kg·d, BPA10 and BPA100) and examined offspring on postnatal days (P) P0, P21, P30, and P120. BPA10 and BPA100 mice presented lower birth weight than control and subsequently gained weight until day 30. At that age, concentration of plasma insulin, C-peptide, and leptin were increased in BPA-exposed animals in the nonfasting state. Insulin secretion and content were diminished in BPA10 and maintained in BPA100 compared with control. A global gene expression analysis indicated that genes related with cell division were increased in islets from BPA-treated animals. This was associated with an increase in pancreatic β-cell mass at P0, P21, and P30 together with increased β-cell proliferation and decreased apoptosis. On the contrary, at P120, BPA-treated animals presented either equal or decreased β-cell mass compared with control and altered fasting glucose levels. These data suggest that in utero exposure to environmentally relevant doses of BPA alters the expression of genes involved in β-cell growth regulation, incrementing β-cell mass/area, and β-cell proliferation during early life. An excess of insulin signaling during early life may contribute to impaired glucose tolerance during adulthood.

Published
2016

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