Loss of macrophage fatty acid oxidation does not potentiate systemic metabolic dysfunction
| Autor: | Elsie Gonzalez-Hurtado, Ebru S. Selen Alpergin, Samuel L. Collins, Maureen R. Horton, Michael J. Wolfgang, Joseph Choi, Jieun Lee |
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| Rok vydání: | 2017 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Physiology Endocrinology Diabetes and Metabolism Macrophage polarization Mice Transgenic Inflammation Diet High-Fat medicine.disease_cause Mice 03 medical and health sciences Insulin resistance Metabolic Diseases Physiology (medical) Internal medicine medicine Animals Carnitine palmitoyltransferase II Obesity adipocyte protein 2 Beta oxidation Cells Cultured Mice Knockout chemistry.chemical_classification biology Macrophages Fatty Acids Fatty acid Macrophage Activation medicine.disease 030104 developmental biology Endocrinology chemistry Biochemistry biology.protein Interleukin-4 medicine.symptom Oxidation-Reduction Oxidative stress Research Article |
| Zdroj: | American Journal of Physiology-Endocrinology and Metabolism. 312:E381-E393 |
| ISSN: | 1522-1555 0193-1849 |
| DOI: | 10.1152/ajpendo.00408.2016 |
| Popis: | 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 Mϕ-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 Mϕ-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. |
| Databáze: | OpenAIRE |
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