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为糖异生引擎提供更多TORC。

More TORC for the gluconeogenic engine.

作者信息

Cheng Alan, Saltiel Alan R

机构信息

Department of Internal Medicine, Life Sciences Institute, University of Michigan Medical Center, Ann Arbor, 48109, USA.

出版信息

Bioessays. 2006 Mar;28(3):231-4. doi: 10.1002/bies.20375.

Abstract

Hepatic gluconeogenesis plays a key role in the maintenance of glucose homeostasis. The hormone glucagon stimulates this process, whereas insulin and adiponectin are inhibitory. In a recent report, Koo et al identify the transcriptional regulator TORC2 (Transducer of Regulated CREB activity 2) as a pivotal component of the gluconeogenic program.1 Both insulin and AMPK increase the phosphorylation of TORC2, while glucagon suppresses it. This in turn regulates the nuclear/cytoplasmic shuttling of TORC2 and its ability to transactivate gluconeogenic genes. Thus, TORC2 might serve as a gluconeogenic "molecular switch" that senses hormones and cellular energy status.

摘要

肝脏糖异生在维持葡萄糖稳态中起关键作用。激素胰高血糖素刺激这一过程,而胰岛素和脂联素则起抑制作用。在最近的一份报告中,Koo等人确定转录调节因子TORC2(调节CREB活性的转导子2)是糖异生程序的关键组成部分。胰岛素和AMPK都会增加TORC2的磷酸化,而胰高血糖素则会抑制它。这反过来又调节了TORC2在细胞核/细胞质之间的穿梭及其反式激活糖异生基因的能力。因此,TORC2可能作为一种糖异生的“分子开关”,感知激素和细胞能量状态。

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