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Horie, Takahiro; Nakao, Tetsushi; Miyasaka, Yui; Nishino, Tomohiro; Matsumura, Shigenobu; Nakazeki, Fumiko; Ide, Yuya; Kimura, Masahiro; Tsuji, Shuhei; Rodriguez, Randolph Ruiz; Watanabe, Toshimitsu; Yamasaki, Tomohiro; Xu, Sijia; Otani, Chiharu; Miyagawa, Sawa; Matsushita, Kazuki; Sowa, Naoya; Omori, Aoi; Tanaka, Jin; Nishimura, Chika; Nishiga, Masataka; Kuwabara, Yasuhide; Baba, Osamu; Watanabe, Shin; Nishi, Hitoo; Nakashima, Yasuhiro; Picciotto, Marina R; Inoue, Haruhisa; Watanabe, Dai; Nakamura, Kazuhiro; Sasaki, Tsutomu; Kimura, Takeshi; Ono, Koh
Nature communications, 02/2021, Volume: 12, Issue: 1Journal Article
Adaptive thermogenesis is essential for survival, and therefore is tightly regulated by a central neural circuit. Here, we show that microRNA (miR)-33 in the brain is indispensable for adaptive thermogenesis. Cold stress increases miR-33 levels in the hypothalamus and miR-33 mice are unable to maintain body temperature in cold environments due to reduced sympathetic nerve activity and impaired brown adipose tissue (BAT) thermogenesis. Analysis of miR-33 dopamine-β-hydroxylase (DBH)-Cre mice indicates the importance of miR-33 in Dbh-positive cells. Mechanistically, miR-33 deficiency upregulates gamma-aminobutyric acid (GABA) receptor subunit genes such as Gabrb2 and Gabra4. Knock-down of these genes in Dbh-positive neurons rescues the impaired cold-induced thermogenesis in miR-33 DBH-Cre mice. Conversely, increased gene dosage of miR-33 in mice enhances thermogenesis. Thus, miR-33 in the brain contributes to maintenance of BAT thermogenesis and whole-body metabolism via enhanced sympathetic nerve tone through suppressing GABAergic inhibitory neurotransmission. This miR-33-mediated neural mechanism may serve as a physiological adaptive defense mechanism for several stresses including cold stress.
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