Novel advances of adiponectin signal transduction network

脂联素通过脂联素受体1 （AdipoR1）诱导细胞外钙内流，这是随后激活CaMKKb和AMPK、增加PGC-1a表达和增加肌细胞线粒体所必需的。此外，肌肉特异性破坏AdipoR1抑制了脂联素介导的细胞内Ca浓度的增加，并降低了脂联素对CaMKK和AMPK的激活。AdipoR1的抑制还导致PGC-1a表达降低，线粒体含量和酶减少，骨骼肌氧化I型肌纤维减少，这与胰岛素抵抗和运动耐力下降有关（Nature 464: 1313,2010）。肥胖患者脂联素和AdipoR1水平的降低可能与糖尿病患者线粒体功能障碍和胰岛素抵抗有关。

Adiponectin induces extracellular Ca influx by adiponectin receptor 1 (AdipoR1), which was necessary for subsequent activation of CaMKKb and AMPK, increased expression PGC-1a, and increased mitochondria in myocytes. Moreover, muscle-specific disruption of AdipoR1 suppressed the adiponectin-mediated increase in intracellular Ca concentration, and decreased the activation of CaMKK and AMPK by adiponectin. Suppression of AdipoR1 also resulted in decreased PGC-1a expression, decreased mitochondrial content and enzymes, and decreased oxidative type I myofibres in skeletal muscle, which were associated with insulin resistance and decreased exercise endurance (Nature 464 : 1313,2010). Decreased levels of adiponectin and AdipoR1 in obesity may have causal roles in mitochondrial dysfunction and insulin resistance seen in diabetes.