來自脂肪的荷爾蒙“脂肪連接蛋白”參與葡萄糖和脂肪酸代謝的調(diào)控,，具有抗糖尿病和抗動(dòng)脈硬化癥的特性。
用肌肉細(xì)胞中缺失“脂肪連接蛋白”受體AdipoR1i的小鼠所做研究表明,，它們具有胰島素抗性,，對(duì)鍛煉的忍耐力沒有野生型小鼠強(qiáng)。
“脂肪連接蛋白”通過AdipoR1在骨骼肌中誘導(dǎo)細(xì)胞外Ca2+流入,，這是線粒體功能和氧化應(yīng)激（壓力）中所涉及的各種下游信號(hào)作用環(huán)節(jié)的一個(gè)先決條件,。這表明，設(shè)計(jì)用來刺激AdipoR1受體或增加骨骼肌中AdipoR1受體數(shù)量的策略,，對(duì)于與肥胖癥有關(guān)的線粒體機(jī)能障礙,、胰島素抗性和2-型糖尿病的治療可能會(huì)有用。(生物谷Bioon.com)
生物谷推薦原文出處：
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.
