||Fish oil intake induces UCP1 upregulation in brown and white adipose tissue via the sympathetic nervous system.
Kim, Minji ,
Goto, Tsuyoshi ,
Yu, Rina ,
Uchida, Kunitoshi ,
Tominaga, Makoto ,
Kano, Yuriko ,
Takahashi, NobuyukiKawada, Teruo
52015-12-17 , Nature Publishing Group
魚油摂取は交感神経を介して、「脂肪燃焼細胞」を増やす－「魚油」の効果で体脂肪燃焼を促す新メカニズムを解明. 京都大学プレスリリース. 2015-12-18.
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.