Kahn Barbara B, Alquier Thierry, Carling David, Hardie D Grahame
Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215, USA.
Cell Metab. 2005 Jan;1(1):15-25. doi: 10.1016/j.cmet.2004.12.003.
The AMP-activated protein kinase (AMPK) is an evolutionarily conserved sensor of cellular energy status, and recent data demonstrate that it also plays a critical role in systemic energy balance. AMPK integrates nutritional and hormonal signals in peripheral tissues and the hypothalamus. It mediates effects of adipokines (leptin, adiponectin, and possibly resistin) in regulating food intake, body weight, and glucose and lipid homeostasis. AMPK is regulated by upstream kinases of which the tumor suppressor, LKB1, is the first to be identified. Complex signaling networks suggest that AMPK may prevent insulin resistance, in part by inhibiting pathways that antagonize insulin signaling. Through signaling, metabolic, and gene expression effects, AMPK enhances insulin sensitivity and fosters a metabolic milieu that may reduce the risk for obesity and type 2 diabetes.
AMP激活的蛋白激酶（AMPK）是一种在进化上保守的细胞能量状态传感器，最近的数据表明它在全身能量平衡中也起着关键作用。AMPK整合外周组织和下丘脑的营养和激素信号。它介导脂肪因子（瘦素、脂联素，可能还有抵抗素）在调节食物摄入、体重以及葡萄糖和脂质稳态方面的作用。AMPK受上游激酶的调节，其中肿瘤抑制因子LKB1是第一个被鉴定出来的。复杂的信号网络表明，AMPK可能部分通过抑制拮抗胰岛素信号的途径来预防胰岛素抵抗。通过信号传导、代谢和基因表达效应，AMPK增强胰岛素敏感性，并营造一种可能降低肥胖和2型糖尿病风险的代谢环境。
