Loss of macrophage fatty acid oxidation does not potentiate systemic metabolic dysfunction.
Am J Physiol Endocrinol Metab
; 312(5): E381-E393, 2017 05 01.
Article
em En
| MEDLINE
| ID: mdl-28223293
ABSTRACT
Fatty acid oxidation in macrophages has been suggested to play a causative role in high-fat diet-induced metabolic dysfunction, particularly in the etiology of adipose-driven insulin resistance. To understand the contribution of macrophage fatty acid oxidation directly to metabolic dysfunction in high-fat diet-induced obesity, we generated mice with a myeloid-specific knockout of carnitine palmitoyltransferase II (CPT2 MÏ-KO), an obligate step in mitochondrial long-chain fatty acid oxidation. While fatty acid oxidation was clearly induced upon IL-4 stimulation, fatty acid oxidation-deficient CPT2 MÏ-KO bone marrow-derived macrophages displayed canonical markers of M2 polarization following IL-4 stimulation in vitro. In addition, loss of macrophage fatty acid oxidation in vivo did not alter the progression of high-fat diet-induced obesity, inflammation, macrophage polarization, oxidative stress, or glucose intolerance. These data suggest that although IL-4-stimulated alternatively activated macrophages upregulate fatty acid oxidation, fatty acid oxidation is dispensable for macrophage polarization and high-fat diet-induced metabolic dysfunction. Macrophage fatty acid oxidation likely plays a correlative, rather than causative, role in systemic metabolic dysfunction.
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Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Interleucina-4
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Ácidos Graxos
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Ativação de Macrófagos
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Macrófagos
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Doenças Metabólicas
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Obesidade
Limite:
Animals
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article