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Am J Physiol Endocrinol Metab. 2015 May 1;308(9):E756-69. doi: 10.1152/ajpendo.00362.2014. Epub 2015 Feb 24.

Enhanced fatty acid oxidation in adipocytes and macrophages reduces lipid-induced triglyceride accumulation and inflammation.

Author information

1
Department of Biochemistry and Molecular Biology, Institut de Biomedicina de la Universitat de Barcelona, Universitat de Barcelona, Barcelona, Spain; Institut de Biomedicina de la Universitat de Barcelona Fisiopatología de la Obesidad y la Nutrición, Instituto de Salud Carlos III, Madrid, Spain;
2
Endocrinology and Diabetes Unit, Joan XXIII University Hospital, Institut d'Investigació Sanitària Pere i Virgili, Universitat Rovira i Virgili, Tarragona, Spain; Institut de Biomedicina de la Universitat de Barcelona de Diabetes y Enfermedades Metabólicas Asociadas, Instituto de Salud Carlos III, Madrid, Spain;
3
Institut de Biomedicina de la Universitat de Barcelona Fisiopatología de la Obesidad y la Nutrición, Instituto de Salud Carlos III, Madrid, Spain; Instituto de Investigaciones Biomédicas Alberto Sols, Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid, Madrid, Spain;
4
Institut de Biomedicina de la Universitat de Barcelona de Diabetes y Enfermedades Metabólicas Asociadas, Instituto de Salud Carlos III, Madrid, Spain; Pharmacology Unit, Department of Pharmacology and Therapeutic Chemistry and Institut de Biomedicina de la Universitat de Barcelona, Faculty of Pharmacy, University of Barcelona, Barcelona, Spain; and.
5
Institut de Biomedicina de la Universitat de Barcelona Fisiopatología de la Obesidad y la Nutrición, Instituto de Salud Carlos III, Madrid, Spain; Basic Sciences Department, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, Barcelona, Spain.
6
Department of Biochemistry and Molecular Biology, Institut de Biomedicina de la Universitat de Barcelona, Universitat de Barcelona, Barcelona, Spain; Institut de Biomedicina de la Universitat de Barcelona Fisiopatología de la Obesidad y la Nutrición, Instituto de Salud Carlos III, Madrid, Spain; lherrero@ub.edu.

Erratum in

Abstract

Lipid overload in obesity and type 2 diabetes is associated with adipocyte dysfunction, inflammation, macrophage infiltration, and decreased fatty acid oxidation (FAO). Here, we report that the expression of carnitine palmitoyltransferase 1A (CPT1A), the rate-limiting enzyme in mitochondrial FAO, is higher in human adipose tissue macrophages than in adipocytes and that it is differentially expressed in visceral vs. subcutaneous adipose tissue in both an obese and a type 2 diabetes cohort. These observations led us to further investigate the potential role of CPT1A in adipocytes and macrophages. We expressed CPT1AM, a permanently active mutant form of CPT1A, in 3T3-L1 CARΔ1 adipocytes and RAW 264.7 macrophages through adenoviral infection. Enhanced FAO in palmitate-incubated adipocytes and macrophages reduced triglyceride content and inflammation, improved insulin sensitivity in adipocytes, and reduced endoplasmic reticulum stress and ROS damage in macrophages. We conclude that increasing FAO in adipocytes and macrophages improves palmitate-induced derangements. This indicates that enhancing FAO in metabolically relevant cells such as adipocytes and macrophages may be a promising strategy for the treatment of chronic inflammatory pathologies such as obesity and type 2 diabetes.

KEYWORDS:

CPT1; adipocytes; fatty acid oxidation; inflammation; macrophages; obesity; type 2 diabetes

PMID:
25714670
DOI:
10.1152/ajpendo.00362.2014
[Indexed for MEDLINE]
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