| First Author | Gonzalez-Hurtado E | Year | 2017 |
| Journal | Am J Physiol Endocrinol Metab | Volume | 312 |
| Issue | 5 | Pages | E381-E393 |
| PubMed ID | 28223293 | Mgi Jnum | J:243928 |
| Mgi Id | MGI:5912707 | Doi | 10.1152/ajpendo.00408.2016 |
| Citation | Gonzalez-Hurtado E, et al. (2017) Loss of macrophage fatty acid oxidation does not potentiate systemic metabolic dysfunction. Am J Physiol Endocrinol Metab 312(5):E381-E393 |
| abstractText | 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 Mvarphi-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 Mvarphi-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. |
