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PPARβ/δ: A Key Therapeutic Target in Metabolic Disorders

1
Pharmacology Unit, Department of Pharmacology, Toxicology and Therapeutic Chemistry, Institute of Biomedicine of the University of Barcelona (IBUB), Faculty of Pharmacy and Food Sciences, University of Barcelona, 08028 Barcelona, Spain
2
Pediatric Research Institute-Hospital Sant Joan de Déu, 08950 Esplugues de Llobregat, Spain
3
Spanish Biomedical Research Center in Diabetes and Associated Metabolic Diseases (CIBERDEM), Instituto de Salud Carlos III, C/Monforte de Lemos 3-5, Pabellón 11, Planta 0, 28029 Madrid, Spain
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(3), 913; https://doi.org/10.3390/ijms19030913
Received: 29 January 2018 / Revised: 9 March 2018 / Accepted: 17 March 2018 / Published: 20 March 2018
(This article belongs to the Special Issue PPARs in Cellular and Whole Body Energy Metabolism)
Research in recent years on peroxisome proliferator-activated receptor (PPAR)β/δ indicates that it plays a key role in the maintenance of energy homeostasis, both at the cellular level and within the organism as a whole. PPARβ/δ activation might help prevent the development of metabolic disorders, including obesity, dyslipidaemia, type 2 diabetes mellitus and non-alcoholic fatty liver disease. This review highlights research findings on the PPARβ/δ regulation of energy metabolism and the development of diseases related to altered cellular and body metabolism. It also describes the potential of the pharmacological activation of PPARβ/δ as a treatment for human metabolic disorders. View Full-Text
Keywords: PPARβ/δ; obesity; dyslipidaemia; type 2 diabetes mellitus; non-alcoholic fatty liver disease PPARβ/δ; obesity; dyslipidaemia; type 2 diabetes mellitus; non-alcoholic fatty liver disease
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MDPI and ACS Style

Palomer, X.; Barroso, E.; Pizarro-Delgado, J.; Peña, L.; Botteri, G.; Zarei, M.; Aguilar, D.; Montori-Grau, M.; Vázquez-Carrera, M. PPARβ/δ: A Key Therapeutic Target in Metabolic Disorders. Int. J. Mol. Sci. 2018, 19, 913.

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