期刊
OBESITY
卷 25, 期 11, 页码 1881-1884出版社
WILEY
DOI: 10.1002/oby.21982
关键词
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资金
- NIH T32 training grant: Training in Pharmacological Sciences [GM007628]
- NIH T32 training grant: Immunobiology of Blood & Vascular Systems [HL069765]
- American Heart Association [12EIA827]
- Department of Veterans Affairs [5I01BX002195]
- American Diabetes Association [1-17-IBS-140]
- Vanderbilt Ingram Cancer Center [CA68485]
- Vanderbilt Digestive Disease Research Center [DK058404]
- National Cancer Institute/NIH Cancer Center support grant [2P30CA068485-14]
- Vanderbilt Mouse Metabolic Phenotyping Center [5U24DK059637-13]
ObjectiveThe prevalence of obesity continues to rise, and it is understood that regulation of white adipose tissue (WAT) function is important to systemic metabolic homeostasis. Immune cells play a central role in the maintenance of WAT, and their compositions change in number and inflammatory phenotype with the progression of obesity. Because of its energy-burning capabilities, brown adipose tissue (BAT) has become a focus of obesity research. Although novel studies have focused on the function of brown adipocytes in thermogenesis, the tissue as a whole has not been immunologically characterized. MethodsBAT immune cell populations were analyzed by flow cytometry and immunohistochemistry in mice with diet-induced obesity (3, 8, or 16 weeks of diet) and in aged mice (1, 6-7, and 10-15 months). ResultsThe data confirmed the presence of macrophages and eosinophils, as previously reported, and showed that 20% to 30% of the immune cells in BAT were B cells. The number of B cells and eosinophils increased with diet-induced obesity, whereas macrophages decreased. There was no change in number of any immune cell quantified with age. ConclusionsThese studies reveal a novel finding of B220+B cells in BAT and show that BAT immune cell populations change in response to diet-induced obesity.
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