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Lack of TRPV 2 impairs thermogenesis in mouse brown adipose tissue
Author(s) -
Sun Wuping,
Uchida Kunitoshi,
Suzuki Yoshiro,
Zhou Yiming,
Kim Minji,
Takayama Yasunori,
Takahashi Nobuyuki,
Goto Tsuyoshi,
Wakabayashi Shigeo,
Kawada Teruo,
Iwata Yuko,
Tominaga Makoto
Publication year - 2016
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201540819
Subject(s) - okazaki fragments , biology , library science , political science , cell growth , computer science , biochemistry , proliferating cell nuclear antigen , eukaryotic dna replication
Brown adipose tissue ( BAT ), a major site for mammalian non‐shivering thermogenesis, could be a target for prevention and treatment of human obesity. Transient receptor potential vanilloid 2 ( TRPV 2), a Ca 2+ ‐permeable non‐selective cation channel, plays vital roles in the regulation of various cellular functions. Here, we show that TRPV 2 is expressed in brown adipocytes and that mRNA levels of thermogenic genes are reduced in both cultured brown adipocytes and BAT from TRPV 2 knockout ( TRPV 2 KO ) mice. The induction of thermogenic genes in response to β‐adrenergic receptor stimulation is also decreased in TRPV 2 KO brown adipocytes and suppressed by reduced intracellular Ca 2+ concentrations in wild‐type brown adipocytes. In addition, TRPV 2 KO mice have more white adipose tissue and larger brown adipocytes and show cold intolerance, and lower BAT temperature increases in response to β‐adrenergic receptor stimulation. Furthermore, TRPV 2 KO mice have increased body weight and fat upon high‐fat‐diet treatment. Based on these findings, we conclude that TRPV 2 has a role in BAT thermogenesis and could be a target for human obesity therapy.
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