Skip to main content

Obesity-induced reduction of adipose eosinophils is reversed with low-calorie dietary intervention.

Citation
Bolus, W. R., et al. “Obesity-Induced Reduction Of Adipose Eosinophils Is Reversed With Low-Calorie Dietary Intervention.”. Physiological Reports, p. e13919.
Center Vanderbilt University
Author William Reid Bolus, Arion J Kennedy, Alyssa H Hasty
Keywords Adipose tissue, eosinophils, inflammation, macrophages, obesity, weight loss
Abstract

While many studies have characterized the inflammatory disposition of adipose tissue (AT) during obesity, far fewer have dissected how such inflammation resolves during the process of physiological weight loss. In addition, new immune cells, such as the eosinophil, have been discovered as part of the AT immune cell repertoire. We have therefore characterized how AT eosinophils, associated eosinophilic inflammation, and remodeling processes, fluctuate during a dietary intervention in obese mice. Similar to previous reports, we found that obesity induced by high-fat diet feeding reduced the AT eosinophil content. However, upon switching obese mice to a low fat diet, AT eosinophils were restored to lean levels as mice reached the body weight of controls. The rise in AT eosinophils during dietary weight loss was accompanied by reduced macrophage content and inflammatory expression, upregulated tissue remodeling factors, and a more uniformly distributed AT vascular network. Additionally, we show that eosinophils of another metabolically relevant tissue, the liver, did not oscillate with either dietary weight gain or weight loss. This study shows that eosinophil content is differentially regulated among tissues during the onset and resolution of obesity. Furthermore, AT eosinophils correlated with AT remodeling processes during weight loss and thus may play a role in reestablishing AT homeostasis.

Year of Publication
2018
Journal
Physiological reports
Volume
6
Issue
22
Number of Pages
e13919
Date Published
11/2018
ISSN Number
2051-817X
DOI
10.14814/phy2.13919
Alternate Journal
Physiol Rep
PMID
30488596
PMCID
PMC6250927
Download citation