Prdm16 is required for the maintenance of brown adipocyte identity and function in adult mice.
Prdm16 is required for the maintenance of brown adipocyte identity and function in adult mice.
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DOI：
10.1016/j.cmet.2014.03.007
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发表时间：
2014-04-01
期刊：
影响因子：
29
通讯作者：
Seale P
中科院分区：
文献类型：
--
作者：
Harms MJ;Ishibashi J;Wang W;Lim HW;Goyama S;Sato T;Kurokawa M;Won KJ;Seale P
Prdm16是一个转录因子，调节棕色和米色脂肪细胞中的产热基因程序。然而，Prdm16是否需要棕色脂肪组织（BAT）在体内的发展或生理功能一直不清楚。通过分析在棕色脂肪谱系中选择性缺乏Prdm16的小鼠，我们发现Prdm16对胚胎BAT发育是不利的。然而，Prdm16需要在年轻的小鼠中通过招募组蛋白甲基转移酶Ehmt 1来抑制BAT中白色脂肪选择性基因的表达。此外，Prdm16缺乏导致肩胛间BAT产热特征的严重成人发病下降。这导致BAT功能障碍和冷敏感性，但不会使动物易于肥胖。有趣的是，由于Prdm16的消融而导致的棕色脂肪身份的丧失通过同时删除密切相关的Prdm3基因而加速。总之，这些结果表明，Prdm 16和Prdm 3控制出生后BAT的身份和功能。
Prdm16 is a transcription factor that regulates the thermogenic gene program in brown and beige adipocytes. However, whether Prdm16 is required for the development or physiological function of brown adipose tissue (BAT) in vivo has been unclear. By analyzing mice that selectively lacked Prdm16 in the brown adipose lineage, we found that Prdm16 was dispensable for embryonic BAT development. However, Prdm16 was required in young mice to suppress the expression of white fat-selective genes in BAT through recruitment of the histone methyltransferase Ehmt1. Additionally, Prdm16-deficiency caused a severe adult-onset decline in the thermogenic character of interscapular BAT. This resulted in BAT dysfunction and cold sensitivity but did not predispose the animals to obesity. Interestingly, the loss of brown fat identity due to ablation of Prdm16 was accelerated by concurrent deletion of the closely related Prdm3 gene. Together, these results show that Prdm16 and Prdm3 control postnatal BAT identity and function.
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影响因子：
11.8
作者：
Park, Jun Hong;Kang, Hong Jun;Kang, Soo Im;Lee, Ji Eun;Hur, Jamie;Ge, Kai;Mueller, Elisabetta;Li, Hongjie;Lee, Byeong-Chel;Lee, Sean Bong
通讯作者：
Lee, Sean Bong
影响因子：
29
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影响因子：
1.5
作者：
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通讯作者：
Fan, Chen-Ming
影响因子：
23.9
作者：
Goyama, Susumu;Yamamoto, Go;Kurokawa, Mineo
通讯作者：
Kurokawa, Mineo
影响因子：
2.7
作者：
Atit, Radhika;Sgaier, Sema K.;Conlon, Ronald A.
通讯作者：
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