The inhibitory effects of quercetin on obesity and obesity-induced inflammation by regulation of MAPK signaling.
Quercetin is a flavonoid found in fruits, vegetables, leaves and grains. It has inhibitory, antiviral, antiasthma, anticancer and antiinflammatory effects. Research has suggested that obesity is linked to metabolic disorders. In this study, we examined the inhibitory effect of quercetin on lipid accumulation and obesity-induced inflammation using 3T3-L1, RAW264.7, zebrafish and mouse models. Quercetin suppressed protein levels of the key adipogenic factors C/EBPβ, C/EBPα, PPARγ and FABP4 and the TG-synthesis enzymes lipin1, DGAT1 and LPAATθ. Activation of m-TOR and p70S6K, which are related to insulin and adipogenesis, was down-regulated during adipogenesis in 3T3-L1 cells. Recent research suggested that MAPK signaling factors were involved in adipogenesis and inflammation and that the adipokines MCP-1 and TNF-α attracted macrophages into adipose tissue. Our data showed that quercetin inhibited the MAPK signaling factors ERK1/2, JNK and p38MAPK and MCP-1 and TNF-α in adipocytes and macrophages. Quercetin also inhibited secretion of the inflammatory cytokines IL-1β and IL-6 and stimulated that of IL-10, an antiinflammatory cytokine. In this study, we confirmed the inhibitory effects of quercetin in adipogenesis and inflammation using a mouse model. In mice, quercetin reduced body weight (almost 40%) and suppressed expression of adipogenic, lipogenic and inflammation-related cytokines. Our data demonstrated that quercetin inhibits lipid accumulation and obesity-induced inflammation in the cell and animal models. Our study suggested that quercetin may represent a potential therapeutic agent for other metabolic disorders by regulating obesity and obesity-induced inflammation.
Department of Food Science and Biotechnology, CHA University, Seongnam, Kyonggi 463-400, South Korea.
Min-Jung
MJ
Seo
Department of Food Science and Biotechnology, CHA University, Seongnam, Kyonggi 463-400, South Korea.
Yeon-Joo
YJ
Lee
Department of Food Science and Biotechnology, CHA University, Seongnam, Kyonggi 463-400, South Korea.
Ji-Hyun
JH
Hwang
Department of Medicine, Harvard Medical School, Massachusetts General Hospital, Charlestown, MA 02129, USA.
Kui-Jin
KJ
Kim
Department of Food Science and Biotechnology, CHA University, Seongnam, Kyonggi 463-400, South Korea. Electronic address: bylee@cha.ac.kr.
Boo-Yong
BY
Lee
D041721:3T3-L1 Cells / Q000187:drug effects; D050156:Adipogenesis / Q000187:drug effects*; D000818:Animals; D002470:Cell Survival / Q000187:drug effects; D016207:Cytokines / Q000378:metabolism; D059305:Diet, High-Fat / Q000009:adverse effects; D007249:Inflammation / Q000188:drug therapy* / Q000378:metabolism; D050356:Lipid Metabolism / Q000187:drug effects; D050155:Lipogenesis / Q000187:drug effects; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009569:Nitric Oxide / Q000378:metabolism; D009765:Obesity / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D011794:Quercetin / Q000494:pharmacology*; D014157:Transcription Factors / Q000378:metabolism; D015027:Zebrafish / Q000378:metabolism
D016207:Cytokines; D014157:Transcription Factors; D009569:Nitric Oxide; D011794:Quercetin
Adipogenesis; MAPK signaling; Obesity; Obesity-induced inflammation; Quercetin