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Lack of Sterol Regulatory Element Binding Factor-1cImposes Glial Fatty Acid Utilization Leading to Peripheral Neuropathy

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Cermenati, Gaia y Audano, Matteo y Giatti, Silvia y Carozzi, Valentina y Porretta Serapiglia, Carla y Pettinato, Emanuela y Ferri, Cinzia y D'Antonio, Maurizio y De Fabiani, Emma y Crestani, Maurizio y Scuranti, Samuele y Sáez, Enrique y Azcoitia Elías, Iñigo y Calavetti, Guido y García Segura, Luis Miguel y Melcangi, Roberto C. y Caruso, Donatella y Mitro, Nico (2015) Lack of Sterol Regulatory Element Binding Factor-1cImposes Glial Fatty Acid Utilization Leading to Peripheral Neuropathy. Cell Metabolism, 21 (4). pp. 571-583. ISSN 1550-4131

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URL Oficial: https://www.sciencedirect.com/science/article/pii/S1550413115000686?via%3Dihub



Resumen

Myelin is a membrane characterized by high lipid content to facilitate impulse propagation. Changes in myelin fatty acid (FA) composition have been associated with peripheral neuropathy, but the specific role of peripheral nerve FA synthesis in myelin formation and function is poorly understood. We have found that mice lacking sterol regulatory element-binding factor-1c (Srebf1c) have blunted peripheral nerve FA synthesis that results in development of peripheral neuropathy. Srebf1c-null mice develop Remak bundle alterations and hypermyelination of small-caliber fibers that impair nerve function. Peripheral nerves lacking Srebf1c show decreased FA synthesis and glycolytic flux, but increased FA catabolism and mitochondrial function. These metabolic alterations are the result of local accumulation of two endogenous peroxisome proliferator-activated receptor-α (Pparα) ligands, 1-palmitoyl-2-oleyl-sn-glycerol-3-phosphatidylcholine and 1-stearoyl-2-oleyl-sn-glycerol-3-phosphatidylcholine. Treatment with a Pparα antagonist rescues the neuropathy of Srebf1c-null mice. These findings reveal the importance of peripheral nerve FA synthesis to sustain myelin structure and function.


Tipo de documento:Artículo
Palabras clave:Cytology; Fatty acids; Nervous System-Diseases
Materias:Ciencias Biomédicas > Biología > Biología celular
Ciencias Biomédicas > Biología > Neurociencias
Código ID:42008
Depositado:29 Mar 2017 17:00
Última Modificación:13 Feb 2018 17:50

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