Quercetin suppresses immune cell accumulation and improves mitochondrial gene expression in adipose tissue of diet-induced obese mice.
METHODS
To examine the effect of dietary quercetin on the function of epididymal adipose tissue (EAT) in Western diet-induced obese mice.


RESULTS
C57BL/6J mice were fed a control diet; a Western diet high in fat, cholesterol, and sucrose; or the same Western diet containing 0.05% quercetin for 18 weeks. Supplementation with quercetin suppressed the increase in the number of macrophages, the decrease in the ratio of CD4(+) to CD8(+) T cells in EAT, and the elevation of plasma leptin and tumor necrosis factor α levels in mice fed the Western diet. Comprehensive gene expression analysis revealed that quercetin suppressed gene expression associated with the accumulation and activation of immune cells, including macrophages and lymphocytes in EAT. It also improved the expression of the oxidative stress-sensitive transcription factor NFκB, NADPH oxidases, and antioxidant enzymes. Quercetin markedly increased gene expression associated with mitochondrial oxidative phosphorylation and mitochondrial DNA content.


CONCLUSIONS
Quercetin most likely universally suppresses the accumulation and activation of immune cells, including antiinflammatory cells, whereas it specifically increased gene expression associated with mitochondrial oxidative phosphorylation. Suppression of oxidative stress and NFκB activity likely contributed to the prevention of the accumulation and activation of immune cells and resulting chronic inflammation.
National Food Research Institute, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan.
Masuko
M
Kobori
National Food Research Institute, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan.
Yumiko
Y
Takahashi
National Food Research Institute, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan.
Mutsumi
M
Sakurai
National Food Research Institute, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan.
Yukari
Y
Akimoto
Department of Food Business, School of Food, Agricultural and Environmental Sciences, Miyagi University, Sendai, Miyagi, Japan.
Tojiro
T
Tsushida
National Food Research Institute, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan.
Hideaki
H
Oike
National Food Research Institute, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan.
Katsunari
K
Ippoushi
D000273:Adipose Tissue / Q000187:drug effects* / Q000276:immunology; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D059305:Diet, High-Fat / Q000009:adverse effects; D004798:Enzymes / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D050259:Genes, Mitochondrial; D008262:Macrophage Activation / Q000187:drug effects; D008264:Macrophages / Q000187:drug effects*; D008297:Male; D024821:Metabolic Syndrome / Q000188:drug therapy; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D009765:Obesity / Q000188:drug therapy* / Q000209:etiology / Q000276:immunology*; D011794:Quercetin / Q000493:pharmacokinetics / Q000494:pharmacology*
D000975:Antioxidants; D004798:Enzymes; D011794:Quercetin
Adipose tissue; Inflammation; Obesity; Oxidative stress; Quercetin