|Title:||microRNA-33 maintains adaptive thermogenesis via enhanced sympathetic nerve activity|
|Authors:||Horie, Takahiro |
Rodriguez, Randolph Ruiz
Picciotto, Marina R.
Inoue, Haruhisa https://orcid.org/0000-0003-4736-9537 (unconfirmed)
Sasaki, Tsutomu https://orcid.org/0000-0001-8041-1915 (unconfirmed)
|Author's alias:||堀江, 貴裕|
|Keywords:||Experimental models of disease|
|Journal title:||Nature Communications|
|Abstract:||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-33f/f 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)A 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-33f/f 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.|
|Description:||褐色脂肪細胞の燃焼を促す新たなメカニズムを解明 --体の熱産生にマイクロRNA-33が関与--. 京都大学プレスリリース. 2021-02-17.|
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|Appears in Collections:||Journal Articles |
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