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      Fish oil intake induces UCP1 upregulation in brown and white adipose tissue via the sympathetic nervous system

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          Abstract

          Brown adipose tissue (BAT) plays a central role in regulating energy homeostasis, and may provide novel strategies for the treatment of human obesity. BAT-mediated thermogenesis is regulated by mitochondrial uncoupling protein 1 (UCP1) in classical brown and ectopic beige adipocytes, and is controlled by sympathetic nervous system (SNS). Previous work indicated that fish oil intake reduces fat accumulation and induces UCP1 expression in BAT; however, the detailed mechanism of this effect remains unclear. In this study, we investigated the effect of fish oil on energy expenditure and the SNS. Fish oil intake increased oxygen consumption and rectal temperature, with concomitant upregulation of UCP1 and the β3 adrenergic receptor (β3AR), two markers of beige adipocytes, in the interscapular BAT and inguinal white adipose tissue (WAT). Additionally, fish oil intake increased the elimination of urinary catecholamines and the noradrenaline (NA) turnover rate in interscapular BAT and inguinal WAT. Furthermore, the effects of fish oil on SNS-mediated energy expenditure were abolished in transient receptor potential vanilloid 1 (TRPV1) knockout mice. In conclusion, fish oil intake can induce UCP1 expression in classical brown and beige adipocytes via the SNS, thereby attenuating fat accumulation and ameliorating lipid metabolism.

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          Most cited references49

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          Impaired nociception and pain sensation in mice lacking the capsaicin receptor.

          The capsaicin (vanilloid) receptor VR1 is a cation channel expressed by primary sensory neurons of the "pain" pathway. Heterologously expressed VR1 can be activated by vanilloid compounds, protons, or heat (>43 degrees C), but whether this channel contributes to chemical or thermal sensitivity in vivo is not known. Here, we demonstrate that sensory neurons from mice lacking VR1 are severely deficient in their responses to each of these noxious stimuli. VR1-/- mice showed normal responses to noxious mechanical stimuli but exhibited no vanilloid-evoked pain behavior, were impaired in the detection of painful heat, and showed little thermal hypersensitivity in the setting of inflammation. Thus, VR1 is essential for selective modalities of pain sensation and for tissue injury-induced thermal hyperalgesia.
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            The Cloned Capsaicin Receptor Integrates Multiple Pain-Producing Stimuli

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              Impaired Nociception and Pain Sensation in Mice Lacking the Capsaicin Receptor

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                Author and article information

                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group
                2045-2322
                17 December 2015
                2015
                : 5
                : 18013
                Affiliations
                [1 ]Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University , Uji, Kyoto 611-0011, Japan
                [2 ]Research Unit for Physiological Chemistry, Kyoto University , Kyoto 606-8501, Japan
                [3 ]Department of Food Science and Nutrition, University of Ulsan , Ulsan 680-749, South Korea
                [4 ]Division of Cell Signaling, Okazaki Institute for Integrative Bioscience (National Institute for Physiological Sciences), National Institutes of Natural Sciences , Okazaki, Aichi 444-8787, Japan
                [5 ]Department of Physiological Sciences, The Graduate University for Advanced Studies , Shonan Village, Hayama, Kanagawa 240-0193, Japan
                [6 ]Laboratory of Nutrition Chemistry, Faculty of Home Economics, Kobe Women’s University , Kobe 654-8585, Japan
                Author notes
                Article
                srep18013
                10.1038/srep18013
                4682086
                26673120
                908c3b36-c001-47a9-8410-6ed00ba143b5
                Copyright © 2015, Macmillan Publishers Limited

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                : 01 April 2015
                : 10 November 2015
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