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Juárez-Flores DL, Ezquerra M, Gonzàlez-Casacuberta Ï, et al. Disrupted Mitochondrial and Metabolic Plasticity Underlie Comorbidity between Age-Related and Degenerative Disorders as Parkinson Disease and Type 2 Diabetes Mellitus. Antioxidants (Basel). 2020;9(11)doi: 10.3390/antiox9111063.
Juárez-Flores, D. L., Ezquerra, M., Gonzàlez-Casacuberta, �. �., Ormazabal, A., Morén, C., Tolosa, E., Fucho, R., Guitart-Mampel, M., Casado, M., Valldeoriola, F., de la Torre-Lara, J., Muñoz, E., Tobías, E., Compta, Y., García-García, F. J., García-Ruiz, C., Fernandez-Checa, J. C., Martí, M. J., Grau, J. M., Cardellach, F., Artuch, R., Fernández-Santiago, R., & Garrabou, G. (2020). Disrupted Mitochondrial and Metabolic Plasticity Underlie Comorbidity between Age-Related and Degenerative Disorders as Parkinson Disease and Type 2 Diabetes Mellitus. Antioxidants (Basel, Switzerland), 9(11), . https://doi.org/10.3390/antiox9111063
Juárez-Flores, Diana Luz, et al. "Disrupted Mitochondrial and Metabolic Plasticity Underlie Comorbidity between Age-Related and Degenerative Disorders as Parkinson Disease and Type 2 Diabetes Mellitus." Antioxidants (Basel, Switzerland) vol. 9,11 (2020). doi: https://doi.org/10.3390/antiox9111063
Juárez-Flores DL, Ezquerra M, Gonzàlez-Casacuberta Ï, Ormazabal A, Morén C, Tolosa E, Fucho R, Guitart-Mampel M, Casado M, Valldeoriola F, de la Torre-Lara J, Muñoz E, Tobías E, Compta Y, García-García FJ, García-Ruiz C, Fernandez-Checa JC, Martí MJ, Grau JM, Cardellach F, Artuch R, Fernández-Santiago R, Garrabou G. Disrupted Mitochondrial and Metabolic Plasticity Underlie Comorbidity between Age-Related and Degenerative Disorders as Parkinson Disease and Type 2 Diabetes Mellitus. Antioxidants (Basel). 2020 Oct 30;9(11). doi: 10.3390/antiox9111063. PMID: 33143119; PMCID: PMC7693963.
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Antioxidants (Basel). 2020 Oct 30;9(11). doi: 10.3390/antiox9111063.

Disrupted Mitochondrial and Metabolic Plasticity Underlie Comorbidity between Age-Related and Degenerative Disorders as Parkinson Disease and Type 2 Diabetes Mellitus.

Antioxidants (Basel, Switzerland)

Diana Luz Juárez-Flores, Mario Ezquerra, Ïngrid Gonzàlez-Casacuberta, Aida Ormazabal, Constanza Morén, Eduardo Tolosa, Raquel Fucho, Mariona Guitart-Mampel, Mercedes Casado, Francesc Valldeoriola, Joan de la Torre-Lara, Esteban Muñoz, Ester Tobías, Yaroslau Compta, Francesc Josep García-García, Carmen García-Ruiz, Jose Carlos Fernandez-Checa, Maria José Martí, Josep Maria Grau, Francesc Cardellach, Rafael Artuch, Rubén Fernández-Santiago, Glòria Garrabou

Affiliations

  1. Laboratory of Muscle Research and Mitochondrial Function, Department of Internal Medicine-Hospital Clínic of Barcelona (HCB), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Faculty of Medicine and Health Science, University of Barcelona (UB), 08036 Barcelona, Spain.
  2. Centro de Investigación Biomédica en Red (CIBER) de Enfermedades Raras (CIBERER), 28029 Madrid, Spain.
  3. Laboratory of Parkinson Disease and Other Neurodegenerative Movement Disorders, IDIBAPS, Institut de Neurociències, UB, 08036 Barcelona, Spain.
  4. Centre for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED CB06/05/0018), 28029 Madrid, Spain.
  5. Department of Clinical Biochemistry, Institut de Recerca de Sant Joan de Deu, Esplugues de Llobregat, 08036 Barcelona, Spain.
  6. Parkinson Disease and Movement Disorders Unit, Neurology Service, HCB, IDIBAPS, UB, 08036 Barcelona, Spain.
  7. Department of Cell Death and Proliferation, Instituto de Investigaciones Biomédicas de Barcelona (IIBB), Consejo Superior Investigaciones Científicas (CSIC), 08001 Barcelona, Spain.
  8. Liver Unit-HCB, IDIBAPS, 08036 Barcelona, Spain.
  9. USC Research Centre for ALPD, Keck School of Medicine, Los Angeles, CA 90033, USA.

PMID: 33143119 PMCID: PMC7693963 DOI: 10.3390/antiox9111063

Abstract

Idiopathic Parkinson's disease (iPD) and type 2 diabetes mellitus (T2DM) are chronic, multisystemic, and degenerative diseases associated with aging, with eventual epidemiological co-morbidity and overlap in molecular basis. This study aims to explore if metabolic and mitochondrial alterations underlie the previously reported epidemiologic and clinical co-morbidity from a molecular level. To evaluate the adaptation of iPD to a simulated pre-diabetogenic state, we exposed primary cultured fibroblasts from iPD patients and controls to standard (5 mM) and high (25 mM) glucose concentrations to further characterize metabolic and mitochondrial resilience. iPD fibroblasts showed increased organic and amino acid levels related to mitochondrial metabolism with respect to controls, and these differences were enhanced in high glucose conditions (citric, suberic, and sebacic acids levels increased, as well as alanine, glutamate, aspartate, arginine, and ornithine amino acids;

Keywords: T2DM (type 2 diabetes mellitus); iPD (idiopathic Parkinson’s disease); metabolome; mitochondria

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