来自脂肪的荷尔蒙“脂肪连接蛋白”参与葡萄糖和脂肪酸代谢的调控，具有抗糖尿病和抗动脉硬化症的特性。
用肌肉细胞中缺失“脂肪连接蛋白”受体AdipoR1i的小鼠所做研究表明，它们具有胰岛素抗性，对锻炼的忍耐力没有野生型小鼠强。
“脂肪连接蛋白”通过AdipoR1在骨骼肌中诱导细胞外Ca2+流入，这是线粒体功能和氧化应激（压力）中所涉及的各种下游信号作用环节的一个先决条件。这表明，设计用来刺激AdipoR1受体或增加骨骼肌中AdipoR1受体数量的策略，对于与肥胖症有关的线粒体机能障碍、胰岛素抗性和2-型糖尿病的治疗可能会有用。
生物谷推荐原文出处：
Nature doi:10.1038/nature08991
Adiponectin and AdipoR1 regulate PGC-1α and mitochondria by Ca2+ and AMPK/SIRT1
Masato Iwabu,Toshimasa Yamauchi,Miki Okada-Iwabu,Koji Sato,Tatsuro Nakagawa,Masaaki Funata,Mamiko Yamaguchi,Shigeyuki Namiki,Ryo Nakayama,Mitsuhisa Tabata,Hitomi Ogata,Naoto Kubota,Iseki Takamoto,Yukiko K. Hayashi,Naoko Yamauchi,Hironori Waki,Masashi Fukayama,Ichizo Nishino,Kumpei Tokuyama,Kohjiro Ueki,Yuichi Oike,Satoshi Ishii,Kenzo Hirose,Takao Shimizu,Kazushige Touhara" Takashi Kadowaki et al.
Adiponectin is an anti-diabetic adipokine. Its receptors possess a seven-transmembrane topology with the amino terminus located intracellularly, which is the opposite of G-protein-coupled receptors. Here we provide evidence that adiponectin induces extracellular Ca2+ influx by adiponectin receptor 1 (AdipoR1), which was necessary for subsequent activation of Ca2+/calmodulin-dependent protein kinase kinase β (CaMKKβ), AMPK and SIRT1, increased expression and decreased acetylation of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), and increased mitochondria in myocytes. Moreover, muscle-specific disruption of AdipoR1 suppressed the adiponectin-mediated increase in intracellular Ca2+ concentration, and decreased the activation of CaMKK, AMPK and SIRT1 by adiponectin. Suppression of AdipoR1 also resulted in decreased PGC-1α expression and deacetylation, decreased mitochondrial content and enzymes, decreased oxidative type I myofibres, and decreased oxidative stress-detoxifying enzymes in skeletal muscle, which were associated with insulin resistance and decreased exercise endurance. Decreased levels of adiponectin and AdipoR1 in obesity may have causal roles in mitochondrial dysfunction and insulin resistance seen in diabetes.
