Lin Jean Z, Farmer Stephen R
Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Genes Dev. 2016 Aug 15;30(16):1793-5. doi: 10.1101/gad.288720.116.
In this issue of Genes & Development, Zeng and colleagues (pp. 1822-1836) identify lysine-specific demethylase 1 (LSD1) as a pivotal regulator of whole-body energy expenditure by controlling the oxidative and thermogenic activity of brown adipose tissue (BAT). They show that LSD1 interacts with PRDM16 to repress select white adipose tissue (WAT) genes but also represses hydroxysteroid 11-β-dehydrogenase 1 (HSD11B1) independently of PRDM16 to prevent production of glucocorticoids that impair BAT functions. Their study provides important insight into epigenetic mechanisms regulating the function of BAT.
在本期《基因与发育》杂志中，曾及其同事（第1822 - 1836页）通过控制棕色脂肪组织（BAT）的氧化和产热活性，确定赖氨酸特异性去甲基化酶1（LSD1）是全身能量消耗的关键调节因子。他们发现，LSD1与PRDM16相互作用以抑制特定的白色脂肪组织（WAT）基因，但也独立于PRDM16抑制11-β-羟基类固醇脱氢酶1（HSD11B1），以防止产生损害BAT功能的糖皮质激素。他们的研究为调节BAT功能的表观遗传机制提供了重要见解。
