线粒体生物发生
安普克
胰岛素抵抗
生物发生
线粒体
AMP活化蛋白激酶
骨骼肌
内分泌学
小檗碱
内科学
细胞生物学
细胞器生物发生
蛋白激酶A
化学
胰岛素
生物
激酶
医学
生物化学
基因
作者
Ana P. Gomes,Filipe V. Duarte,Patrícia M. Nunes,Basil P. Hubbard,João S. Teodoro,Ana Varela,John G. Jones,David A. Sinclair,Carlos M. Palmeira,Anabela P. Rolo
标识
DOI:10.1016/j.bbadis.2011.10.008
摘要
Berberine (BBR) has recently been shown to improve insulin sensitivity in rodent models of insulin resistance. Although this effect was explained partly through an observed activation of AMP-activated protein kinase (AMPK), the upstream and downstream mediators of this phenotype were not explored. Here, we show that BBR supplementation reverts mitochondrial dysfunction induced by High Fat Diet (HFD) and hyperglycemia in skeletal muscle, in part due to an increase in mitochondrial biogenesis. Furthermore, we observe that the prevention of mitochondrial dysfunction by BBR, the increase in mitochondrial biogenesis, as well as BBR-induced AMPK activation, are blocked in cells in which SIRT1 has been knocked-down. Taken together, these data reveal an important role for SIRT1 and mitochondrial biogenesis in the preventive effects of BBR on diet-induced insulin resistance.
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