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Title: Dietary oleic acid increases M2 macrophages in the mesenteric adipose

Author
item CAMELL, CHRISTINA - Baylor College Of Medicine
item SMITH, CLIFTON - Children'S Nutrition Research Center (CNRC)

Submitted to: PLOS ONE
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/13/2013
Publication Date: 9/30/2013
Citation: Camell, C., Smith, C.W. 2013. Dietary oleic acid increases M2 macrophages in the mesenteric adipose. PLoS One. 8(9):e75147.

Interpretive Summary: The fatty tissues in the abdomen change in response to a long term high fat diet. The fat cells increase in size, and white blood cells migrate into these tissues and promote tissue inflammation. The purpose of this study was to determine the effects of a short term high fat diet on white blood cells in the fatty tissues of the abdomen. Our results revealed that, in contrast to the long term diet, mice fed a high fat diet for 3 days increased an anti-inflammatory type of white blood cell in the fatty tissues around the intestines, and that one type of fat in the diet (called oleic acid) was capable of producing this effect. This study raises the possibility of the potential anti-inflammatory benefits of oleic acid.

Technical Abstract: Several studies have implicated fatty-acids as inflammatory regulators, suggesting that there may be a direct role for common dietary fatty-acids in regulating innate immune cells. In humans, a single high-fat meal increases systemic cytokines and leukocytes. In mice, short term high-fat feeding increases adipose tissue leukocytes and alters the inflammatory profile of adipose tissue macrophages. We have seen that short term high fat feeding to C57BL/6J male mice increases palmitic and oleic acid within adipose tissue depots, but oleic acid increase is highest in the mesenteric adipose tissue. In vitro, oleic acid increases M2 macrophage markers (CD206, MGL1, and ARG1) in a murine macrophage cell line, while addition of palmitic acid is able to inhibit that increase. Three day supplementation of a chow diet, with oleic acid, induced an increase in M2 macrophage markers in the mesenteric adipose tissue, but not in the epididymal adipose tissue. We tested whether increases in M2 macrophages occur during short term ad lib feeding of a high fat diet, containing oleic acid. Experiments revealed two distinct populations of macrophages were altered by a three day high milk-fat diet. One population, phenotypically intermediate for F4/80, showed diet-induced increases in CD206, an anti-inflammatory marker characteristic of M2 macrophages intrinsic to the AT. Evidence for a second population, phenotypically F4/80HICD11bHI macrophages, showed increased association with the mesenteric adipose tissue following short term feeding that is dependent on the adhesion molecule, ICAM-1. Collectively, we have shown that short term feeding of a high-fat diet changes two population of macrophages, and that dietary oleic acid is responsible for increases in M2 macrophage polarization.