13 results on '"Gomis, R"'
Search Results
2. Fatty liver index as a predictor for type 2 diabetes in subjects with normoglycemia in a nationwide cohort study
- Author
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García-Escobar, E., Valdés, S., Soriguer, F., Vendrell, J., Urrutia-Etxebarria, I. M., Maldonado-Araque, C., Ortega, E., Ocón, P., Montanya, E., Menéndez, E., Lago-Sampedro, A., González-Frutos, T., Gomis, R., Goday, A., García-Serrano, S., Galán-García, J. L., Castell, C., Bordiú, E., Badía, R., Aguilera-Venegas, G., Girbés, J., Gaztambide, S., Delgado, E., Chaves, F. J., Castaño, L., Calle-Pascual, A., Rojo-Martínez, G., and Franch-Nadal, J.
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- 2021
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3. Our journal is 65 years-old: A look back at the past
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Corcoy, R, Lucas, A, Gomis, R, Mauricio, D, Wagner, A, Jimenez, A, Fajardo, C, Ballesteros, M, Gimeno, JA, and Zafon, C
- Published
- 2022
4. Targeted immunotherapy against distinct cancer-associated fibroblasts overcomes treatment resistance in refractory HER2+breast tumors
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Rivas E, Linares J, Zwick M, Gomez-Llonin A, Guiu M, Labernadie A, Badia-Ramentol J, Llado A, Bardia L, Perez-Nunez I, Martinez-Ciarpaglini C, Tarazona N, Sallent-Aragay A, Garrido M, Celia-Terrassa T, Burgues O, Gomis R, Albanell J, and Calon A
- Abstract
A substantial proportion of HER2+ breast cancer patients do not benefit from HER2-targeted therapy. Here, the authors identify a population of cancer-associated fibroblasts involved in the suppression of trastuzumab-induced ADCC that can be pharmacologically targeted to raise treatment effectiveness in unresponsive tumors. About 50% of human epidermal growth factor receptor 2 (HER2)+ breast cancer patients do not benefit from HER2-targeted therapy and almost 20% of them relapse after treatment. Here, we conduct a detailed analysis of two independent cohorts of HER2+ breast cancer patients treated with trastuzumab to elucidate the mechanisms of resistance to anti-HER2 monoclonal antibodies. In addition, we develop a fully humanized immunocompetent model of HER2+ breast cancer recapitulating ex vivo the biological processes that associate with patients' response to treatment. Thanks to these two approaches, we uncover a population of TGF-beta-activated cancer-associated fibroblasts (CAF) specific from tumors resistant to therapy. The presence of this cellular subset related to previously described myofibroblastic (CAF-S1) and podoplanin+ CAF subtypes in breast cancer associates with low IL2 activity. Correspondingly, we find that stroma-targeted stimulation of IL2 pathway in unresponsive tumors restores trastuzumab anti-cancer efficiency. Overall, our study underscores the therapeutic potential of exploiting the tumor microenvironment to identify and overcome mechanisms of resistance to anti-cancer treatment.
- Published
- 2022
5. Heart rate variability as an indicator of acid gastroesophageal reflux.
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Murcia Clemente, L., Izquierdo Fos, I., Vázquez Gomis, R., López Yánez, A., and Valero Sánchez, M. Á.
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- 2022
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6. Study of factors associated with dietary trangressions in celiacs and analysis of ferritine levels according to adherence to a free gluten-free diet.
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Vázquez-Gomis, R., Vázquez-Acebes, B., Juste-Ruiz, M., Izquierdo-Vázquez, A., and Izquierdo-Fos, I.
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- 2022
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7. Direct reprogramming of human fibroblasts into insulin-producing cells using transcription factors.
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Fontcuberta-PiSunyer M, García-Alamán A, Prades È, Téllez N, Alves-Figueiredo H, Ramos-Rodríguez M, Enrich C, Fernandez-Ruiz R, Cervantes S, Clua L, Ramón-Azcón J, Broca C, Wojtusciszyn A, Montserrat N, Pasquali L, Novials A, Servitja JM, Vidal J, Gomis R, and Gasa R
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- Humans, Gene Expression Regulation, Cell Differentiation physiology, Fibroblasts metabolism, Transcription Factors genetics, Transcription Factors metabolism, Insulin metabolism
- Abstract
Direct lineage reprogramming of one somatic cell into another without transitioning through a progenitor stage has emerged as a strategy to generate clinically relevant cell types. One cell type of interest is the pancreatic insulin-producing β cell whose loss and/or dysfunction leads to diabetes. To date it has been possible to create β-like cells from related endodermal cell types by forcing the expression of developmental transcription factors, but not from more distant cell lineages like fibroblasts. In light of the therapeutic benefits of choosing an accessible cell type as the cell of origin, in this study we set out to analyze the feasibility of transforming human skin fibroblasts into β-like cells. We describe how the timed-introduction of five developmental transcription factors (Neurog3, Pdx1, MafA, Pax4, and Nkx2-2) promotes conversion of fibroblasts toward a β-cell fate. Reprogrammed cells exhibit β-cell features including β-cell gene expression and glucose-responsive intracellular calcium mobilization. Moreover, reprogrammed cells display glucose-induced insulin secretion in vitro and in vivo. This work provides proof-of-concept of the capacity to make insulin-producing cells from human fibroblasts via transcription factor-mediated direct reprogramming., (© 2023. The Author(s).)
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- 2023
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8. Remission of obesity and insulin resistance is not sufficient to restore mitochondrial homeostasis in visceral adipose tissue.
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Gonzalez-Franquesa A, Gama-Perez P, Kulis M, Szczepanowska K, Dahdah N, Moreno-Gomez S, Latorre-Pellicer A, Fernández-Ruiz R, Aguilar-Mogas A, Hoffman A, Monelli E, Samino S, Miró-Blanch J, Oemer G, Duran X, Sanchez-Rebordelo E, Schneeberger M, Obach M, Montane J, Castellano G, Chapaprieta V, Sun W, Navarro L, Prieto I, Castaño C, Novials A, Gomis R, Monsalve M, Claret M, Graupera M, Soria G, Wolfrum C, Vendrell J, Fernández-Veledo S, Enríquez JA, Carracedo A, Perales JC, Nogueiras R, Herrero L, Trifunovic A, Keller MA, Yanes O, Sales-Pardo M, Guimerà R, Blüher M, Martín-Subero JI, and Garcia-Roves PM
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- Adipose Tissue metabolism, Animals, Homeostasis, Intra-Abdominal Fat metabolism, Mice, Obesity genetics, Obesity metabolism, Proteomics, Insulin Resistance
- Abstract
Metabolic plasticity is the ability of a biological system to adapt its metabolic phenotype to different environmental stressors. We used a whole-body and tissue-specific phenotypic, functional, proteomic, metabolomic and transcriptomic approach to systematically assess metabolic plasticity in diet-induced obese mice after a combined nutritional and exercise intervention. Although most obesity and overnutrition-related pathological features were successfully reverted, we observed a high degree of metabolic dysfunction in visceral white adipose tissue, characterized by abnormal mitochondrial morphology and functionality. Despite two sequential therapeutic interventions and an apparent global healthy phenotype, obesity triggered a cascade of events in visceral adipose tissue progressing from mitochondrial metabolic and proteostatic alterations to widespread cellular stress, which compromises its biosynthetic and recycling capacity. In humans, weight loss after bariatric surgery showed a transcriptional signature in visceral adipose tissue similar to our mouse model of obesity reversion. Overall, our data indicate that obesity prompts a lasting metabolic fingerprint that leads to a progressive breakdown of metabolic plasticity in visceral adipose tissue., (Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.)
- Published
- 2022
- Full Text
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9. Glycaemia Fluctuations Improvement in Old-Age Prediabetic Subjects Consuming a Quinoa-Based Diet: A Pilot Study.
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Díaz-Rizzolo DA, Acar-Denizli N, Kostov B, Roura E, Sisó-Almirall A, Delicado P, and Gomis R
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- Blood Glucose metabolism, Cross-Over Studies, Diet, Humans, Pilot Projects, Chenopodium quinoa, Diabetes Mellitus, Type 2 prevention & control, Prediabetic State
- Abstract
This study aimed to observe if quinoa could produce a benefit on postprandial glycemia that would result in less progression to type 2 diabetes (T2D). A cross-over design pilot clinical study with a nutritional intervention for 8 weeks was performed: 4 weeks on a regular diet (RD) and 4 weeks on a quinoa diet (QD). Nine subjects aged ≥65 years with prediabetes were monitored during the first 4 weeks of RD with daily dietary records and FreeStyle Libre®. Subsequently, participants started the QD, where quinoa and 100% quinoa-based products replaced foods rich in complex carbohydrates that they had consumed in the first 4 weeks of RD. The glycemic measurements recorded by the sensors were considered as functions of time, and the effects of nutrients consumed at the intended time period were analyzed by means of a function-on-scalar regression (fosr) model. With QD participants, decreased body weight (−1.6 kg, p = 0.008), BMI (−0.6 kg/m2p = 0.004) and waist circumference (−1.5 cm, p = 0.015) were observed. Nutrients intake changed during QD, namely, decreased carbohydrates (p = 0.004) and increased lipids (p = 0.004) and some amino acids (p < 0.05). The fosr model showed a reduction in postprandial glycemia in QD despite intrapersonal differences thanks to the joint action of different nutrients and the suppression of others consumed on a regular diet. We conclude that in an old age and high T2D-risk population, a diet rich in quinoa reduces postprandial glycemia and could be a promising T2D-preventive strategy.
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- 2022
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10. Our journal is 65 years-old (I): A look back at the past.
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Corcoy R, Lucas A, Gomis R, Mauricio D, Wägner A, Jiménez A, Fajardo C, Ballesteros M, Gimeno JA, and Zafon C
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- 2022
- Full Text
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11. Low Percentage of Vegetable Fat in Red Blood Cells Is Associated with Worse Glucose Metabolism and Incidence of Type 2 Diabetes.
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Chiva-Blanch G, Giró O, Cofán M, Calle-Pascual AL, Delgado E, Gomis R, Jiménez A, Franch-Nadal J, Rojo Martínez G, and Ortega E
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- Adult, Docosahexaenoic Acids, Eicosapentaenoic Acid, Erythrocytes metabolism, Fatty Acids, Female, Glucose analysis, Humans, Incidence, Linoleic Acid, Male, Middle Aged, Vegetables metabolism, alpha-Linolenic Acid, Diabetes Mellitus, Type 2 epidemiology, Diabetes Mellitus, Type 2 etiology, Fatty Acids, Omega-3 analysis
- Abstract
The identification of nutritional patterns associated with the development of type 2 diabetes (T2D) might help lead the way to a more efficient and personalized nutritional intervention. Our study is aimed at evaluating the association between fatty acids (FA) in red blood cell (RBC) membranes, as a quantitative biomarker of regular dietary fat intake, and incident type 2 diabetes in a Spanish population. We included 1032 adult Spaniards (57% women, age 49 ± 15 years, 18% prediabetes), without diabetes at study entry, from the Di@bet.es cohort. Incident diabetes was diagnosed at the end of the study follow-up. The FA percentage in RBC was determined at baseline by gas chromatography. Participants were followed on average 7.5 ± 0.6 years. Lower percentages of linoleic acid (LA), α-linolenic (ALA), and eicosapentaenoic acid (EPA), and higher percentages of docosahexaenoic acid (DHA) in RBC membranes were associated, independently of classical risk factors, with worse glucose metabolism at the end of the study follow-up. In addition, higher percentages of ALA and EPA, and moderate percentages of DHA, were associated with lower risk of diabetes. No significant associations were found for LA and diabetes risk. Dietary patterns rich in vegetables are independently associated with lower risk of both deterioration of glucose regulation and incident diabetes, and should be reinforced for the prevention of diabetes.
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- 2022
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12. Gsα-dependent signaling is required for postnatal establishment of a functional β-cell mass.
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Serra-Navarro B, Fernandez-Ruiz R, García-Alamán A, Pradas-Juni M, Fernandez-Rebollo E, Esteban Y, Mir-Coll J, Mathieu J, Dalle S, Hahn M, Ahlgren U, Weinstein LS, Vidal J, Gomis R, and Gasa R
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- Animals, GTP-Binding Protein alpha Subunits, Gs deficiency, Mice, Knockout, Mice, Transgenic, Signal Transduction, Mice, GTP-Binding Protein alpha Subunits, Gs metabolism, Insulin-Secreting Cells metabolism
- Abstract
Objective: Early postnatal life is a critical period for the establishment of the functional β-cell mass that will sustain whole-body glucose homeostasis during the lifetime. β cells are formed from progenitors during embryonic development but undergo significant expansion in quantity and attain functional maturity after birth. The signals and pathways involved in these processes are not fully elucidated. Cyclic adenosine monophosphate (cAMP) is an intracellular signaling molecule that is known to regulate insulin secretion, gene expression, proliferation, and survival of adult β cells. The heterotrimeric G protein Gs stimulates the cAMP-dependent pathway by activating adenylyl cyclase. In this study, we sought to explore the role of Gs-dependent signaling in postnatal β-cell development., Methods: To study Gs-dependent signaling, we generated conditional knockout mice in which the α subunit of the Gs protein (Gsα) was ablated from β-cells using the Cre deleter line Ins1
Cre . Mice were characterized in terms of glucose homeostasis, including in vivo glucose tolerance, glucose-induced insulin secretion, and insulin sensitivity. β-cell mass was studied using histomorphometric analysis and optical projection tomography. β-cell proliferation was studied by ki67 and phospho-histone H3 immunostatining, and apoptosis was assessed by TUNEL assay. Gene expression was determined in isolated islets and sorted β cells by qPCR. Intracellular cAMP was studied in isolated islets using HTRF-based technology. The activation status of the cAMP and insulin-signaling pathways was determined by immunoblot analysis of the relevant components of these pathways in isolated islets. In vitro proliferation of dissociated islet cells was assessed by BrdU incorporation., Results: Elimination of Gsα in β cells led to reduced β-cell mass, deficient insulin secretion, and severe glucose intolerance. These defects were evident by weaning and were associated with decreased proliferation and inadequate expression of key β-cell identity and maturation genes in postnatal β-cells. Additionally, loss of Gsα caused a broad multilevel disruption of the insulin transduction pathway that resulted in the specific abrogation of the islet proliferative response to insulin., Conclusion: We conclude that Gsα is required for β-cell growth and maturation in the early postnatal stage and propose that this is partly mediated via its crosstalk with insulin signaling. Our findings disclose a tight connection between these two pathways in postnatal β cells, which may have implications for using cAMP-raising agents to promote β-cell regeneration and maturation in diabetes., (Copyright © 2021 The Author(s). Published by Elsevier GmbH.. All rights reserved.)- Published
- 2021
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13. Mitochondrial cristae-remodeling protein OPA1 in POMC neurons couples Ca 2+ homeostasis with adipose tissue lipolysis.
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Gómez-Valadés AG, Pozo M, Varela L, Boudjadja MB, Ramírez S, Chivite I, Eyre E, Haddad-Tóvolli R, Obri A, Milà-Guasch M, Altirriba J, Schneeberger M, Imbernón M, Garcia-Rendueles AR, Gama-Perez P, Rojo-Ruiz J, Rácz B, Alonso MT, Gomis R, Zorzano A, D'Agostino G, Alvarez CV, Nogueiras R, Garcia-Roves PM, Horvath TL, and Claret M
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- Adipose Tissue metabolism, Animals, GTP Phosphohydrolases, Homeostasis, Mice, Neurons metabolism, Lipolysis, Pro-Opiomelanocortin metabolism
- Abstract
Appropriate cristae remodeling is a determinant of mitochondrial function and bioenergetics and thus represents a crucial process for cellular metabolic adaptations. Here, we show that mitochondrial cristae architecture and expression of the master cristae-remodeling protein OPA1 in proopiomelanocortin (POMC) neurons, which are key metabolic sensors implicated in energy balance control, is affected by fluctuations in nutrient availability. Genetic inactivation of OPA1 in POMC neurons causes dramatic alterations in cristae topology, mitochondrial Ca
2+ handling, reduction in alpha-melanocyte stimulating hormone (α-MSH) in target areas, hyperphagia, and attenuated white adipose tissue (WAT) lipolysis resulting in obesity. Pharmacological blockade of mitochondrial Ca2+ influx restores α-MSH and the lipolytic program, while improving the metabolic defects of mutant mice. Chemogenetic manipulation of POMC neurons confirms a role in lipolysis control. Our results unveil a novel axis that connects OPA1 in POMC neurons with mitochondrial cristae, Ca2+ homeostasis, and WAT lipolysis in the regulation of energy balance., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)- Published
- 2021
- Full Text
- View/download PDF
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