10‐oxo‐12(Z)‐octadecenoic acid, a linoleic acid metabolite produced by gut lactic acid bacteria, enhances energy metabolism by activation of TRPV1. Issue 11 (28th July 2017)

• Record Type: Journal Article
• Authors: Kim, Minji; Furuzono, Tomoya; Yamakuni, Kanae; Li, Yongjia; Kim, Young‐Il; Takahashi, Haruya; Ohue‐Kitano, Ryuji; Jheng, Huei‐Fen; Takahashi, Nobuyuki; Kano, Yuriko; Yu, Rina; Kishino, Shigenobu; Ogawa, Jun; Uchida, Kunitoshi; Yamazaki, Jun; Tominaga, Makoto; Kawada, Teruo; Goto, Tsuyoshi
• Is Part Of: FASEB journal. Volume 31:Issue 11(2017)
• Page Start: 5036
• Page End: 5048
• Publication Date: 2017-07-28
• Subjects: UCP1 -- beige cells -- fatty acids -- gut microbiota -- obesity; Biology -- Periodicals; Biology, Experimental -- Periodicals; 570
• DOI: 10.1096/fj.201700151R
• Languages: English
• ISSNs: 0892-6638

Abstract

Abstract : Gut microbiota can regulate the host energy metabolism; however, the underlying mechanisms that could involve gut microbiota–derived compounds remain to be understood. Therefore, in this study, we investigated the effects of KetoA [10‐oxo‐12( Z )‐octadecenoic acid]—a linoleic acid metabolite produced by gut lactic acid bacteria—on whole‐body energy metabolism and found that dietary intake of KetoA could enhance energy expenditure in mice, thereby protecting mice from diet‐induced obesity. By using Ca 2+ imaging and whole‐cell patch‐clamp methods, KetoA was noted to potently activate transient receptor potential vanilloid 1 (TRPV1) and enhance noradrenalin turnover in adipose tissues. In addition, KetoA up‐regulated genes that are related to brown adipocyte functions, including uncoupling protein 1 (UCP1) in white adipose tissue (WAT), which was later diminished in the presence of a β‐adrenoreceptor blocker. By using obese and diabetic model KK‐Ay mice, we further show that KetoA intake ameliorated obesity‐associated metabolic disorders. In the absence of any observed KetoA‐induced antiobesity effect or UCP1 up‐regulation in TRPV1‐deficient mice, we prove that the antiobesity effect of KetoA was caused by TRPV1 activation‐mediated browning in WAT. KetoA produced in the gut could therefore be involved in the regulation of host energy metabolism.—Kim, M., Furuzono, T., Yamakuni, K., Li, Y., Kim, Y.‐I., Takahashi, H., Ohue‐Kitano, R., Jheng, H.‐F., Takahashi, N., Kano, Y., Yu, R., Kishino, S., Ogawa, J., Uchida, K., Yamazaki, J., Tominaga, M., Kawada, T., Goto, T. 10‐oxo‐12(Z)‐octadecenoic acid, a linoleic acid metabolite produced by gut lactic acid bacteria, enhances energy metabolism by activation of TRPV1. FASEB J. 31, 5036–5048 (2017). www.fasebj.org