Mitochondria-associated endoplasmic reticulum membranes allow adaptation of mitochondrial metabolism to glucose availability in the liver
| Autor: | Emily Tubbs, Muriel Le Romancer, Nadia BENDRIDI, Jennifer Rieusset, Guillaume Vial, Julien Jacquemetton, Team1 Carmen, Hubert VIDAL, Muhammad Rizwan Alam, Team2 Carmen, Carmen Lab, Marie-Agnes BERGER |
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| Přispěvatelé: | Cardiovasculaire, métabolisme, diabétologie et nutrition (CarMeN), Institut National de la Recherche Agronomique (INRA)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hospices Civils de Lyon (HCL), Centre de Recherche en Cancérologie de Lyon (CRCL), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Université de Lyon-Institut National des Sciences Appliquées (INSA)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Institut National de la Recherche Agronomique (INRA), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), INSERM, the national research agency ANR-09-JCJC-0116, French government of higher education and research, Fondation pour la Recherche Medicale FDT20140931004, Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM) |
| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
medicine.medical_treatment [SDV]Life Sciences [q-bio] pentose phosphate pathway Nutritional Status Mitochondrion Endoplasmic Reticulum Diabetes Mellitus Experimental Mice 03 medical and health sciences Insulin resistance mitochondria dynamic Phosphoprotein Phosphatases hepatocyte Genetics medicine Animals Humans Inositol 1 4 5-Trisphosphate Receptors Molecular Biology Cyclophilin Mice Knockout glucose sensing Chemistry Voltage-Dependent Anion Channel 1 Insulin Endoplasmic reticulum Intracellular Membranes Cell Biology General Medicine Postprandial Period medicine.disease Mitochondria PP2A Cell biology Glucose 030104 developmental biology Liver MAM Hepatocytes Microsome Mitochondrial fission Signal transduction Signal Transduction |
| Zdroj: | Journal of molecular cell biology Journal of molecular cell biology, Oxford UP, 2016, 8 (2), pp.129-43. ⟨10.1093/jmcb/mjw004⟩ |
| ISSN: | 1674-2788 1759-4685 |
| DOI: | 10.1093/jmcb/mjw004⟩ |
| Popis: | International audience; Mitochondria-associated endoplasmic reticulum membranes (MAM) play a key role in mitochondrial dynamics and function and in hepatic insulin action. Whereas mitochondria are important regulators of energy metabolism, the nutritional regulation of MAM in the liver and its role in the adaptation of mitochondria physiology to nutrient availability are unknown. In this study, we found that the fasted to postprandial transition reduced the number of endoplasmic reticulum-mitochondria contact points in mouse liver. Screening of potential hormonal/metabolic signals revealed glucose as the main nutritional regulator of hepatic MAM integrity both in vitro and in vivo Glucose reduced organelle interactions through the pentose phosphate-protein phosphatase 2A (PP-PP2A) pathway, induced mitochondria fission, and impaired respiration. Blocking MAM reduction counteracted glucose-induced mitochondrial alterations. Furthermore, disruption of MAM integrity mimicked effects of glucose on mitochondria dynamics and function. This glucose-sensing system is deficient in the liver of insulin-resistant ob/ob and cyclophilin D-KO mice, both characterized by chronic disruption of MAM integrity, mitochondrial fission, and altered mitochondrial respiration. These data indicate that MAM contribute to the hepatic glucose-sensing system, allowing regulation of mitochondria dynamics and function during nutritional transition. Chronic disruption of MAM may participate in hepatic mitochondrial dysfunction associated with insulin resistance. |
| Databáze: | OpenAIRE |
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