Research Article Quercetin Protects against Obesity-Induced Skeletal Muscle Inflammation and Atrophy Ngoc Hoan Le, 1 Chu-Sook Kim, 1 Taesun Park, 2 Jung Han Yoon Park, 3 Mi-Kyung Sung, 4 Dong Gun Lee, 5 Sun-Myung Hong, 1 Suck-Young Choe, 1 Tsuyoshi Goto, 6 Teruo Kawada, 6 and Rina Yu 1 1 Department of Food Science and Nutrition, University of Ulsan, Ulsan 680-749, Republic of Korea 2 Department of Food and Nutrition, Yonsei University, Seoul 120-749, Republic of Korea 3 Department of Food Science and Nutrition and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 200-702, Republic of Korea 4 Sookmyung Women’s University, Seoul 140-742, Republic of Korea 5 School of Life Science and Biotechnology, Kyungpook National University, Daegu 702-701, Republic of Korea 6 Graduate School of Agriculture, Kyoto University, Uji, Kyoto 611-0011, Japan Correspondence should be addressed to Rina Yu; rinayu@ulsan.ac.kr Received 17 September 2014; Revised 22 November 2014; Accepted 23 November 2014; Published 28 December 2014 Academic Editor: Giuseppe Valacchi Copyright © 2014 Ngoc Hoan Le et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Skeletal muscle infammation and atrophy are closely associated with metabolic impairment such as insulin resistance. Quercetin, a natural polyphenol favonoid, is known to elicit anti-infammatory and antioxidant activities. In this study, we investigated its efect on obesity-induced skeletal muscle infammation and atrophy in mice. Male C57BL/6 mice were fed a regular diet, a high- fat diet (HFD), and an HFD supplemented with quercetin for nine weeks. Quercetin reduced levels of infammatory cytokines and macrophage accumulation in the skeletal muscle of the HFD-fed obese mice. It also reduced transcript and protein levels of the specifc atrophic factors, Atrogin-1 and MuRF1, in the skeletal muscle of the HFD-fed obese mice, and protected against the reduction of muscle mass and muscle fber size. In vitro, quercetin markedly diminished transcript levels of infammatory receptors and activation of their signaling molecules (ERK, p38 MAPK, and NF-B) in cocultured myotubes/macrophages, and this was accompanied by reduced expression of the atrophic factors. Together, these fndings suggest that quercetin reduces obesity-induced skeletal muscle atrophy by inhibiting infammatory receptors and their signaling pathway. Quercetin may be useful for preventing obesity-induced muscle infammation and sarcopenia. 1. Introduction Skeletal muscle is the most abundant tissue, with a wide variety of physiological functions, and thus muscle loss results not only in physical dysfunction but also in metabolic impairment [1]. Infammatory mediators such as tumor necrosis factor alpha (TNF) and interleukin-6 (IL-6) are important mediators of catabolic responses such as protein loss and of metabolic disturbances such as insulin resistance [2]. Tey promote protein degradation by upregulating the expression of two muscle-specifc ubiquitin E3-ligases, F-box protein (MAFbx/Atrogin-1), and muscle ring-fnger protein 1 (MuRF1), which are involved in the ubiquitin proteasome pathway, and so lead to skeletal muscle atrophy [3]. Recent studies have shown that obesity is associated with skeletal muscle loss and dysfunction, referred to as sarcopenic obesity [4]. It is likely that obesity-induced infammation, which is characterized by increases in macrophage infltration and in levels of infammatory cytokines/chemokines (e.g., TNF; monocyte chemoattractant protein 1, MCP-1) [5–7], is asso- ciated with this muscle atrophy. Given that muscle atrophy and infammation exacerbate obesity-induced insulin resis- tance [8], dietary components that suppress obesity-induced skeletal muscle infammation and/or atrophy could be useful for preventing obesity-related metabolic disorders. Hindawi Publishing Corporation Mediators of Inflammation Volume 2014, Article ID 834294, 10 pages http://dx.doi.org/10.1155/2014/834294