Loss of macrophage fatty acid oxidation does not potentiate systemic metabolic dysfunction

Elsie Gonzalez-Hurtado, Jieun Lee, Joseph Choi, Ebru S. Selen Alpergin, Samuel L. Collins, Maureen R. Horton, Michael J. Wolfgang

Research output: Contribution to journalArticle

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 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.

Original languageEnglish (US)
Pages (from-to)E381-E393
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume312
Issue number5
DOIs
StatePublished - May 2017

Keywords

  • Adipose tissue
  • Fatty acid
  • Inflammation
  • Macrophage
  • Obesity

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)

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