Glycogen autophagy in the liver and heart of newborn rats. The effects of glucagon, adrenalin or rapamycin

Glycogen autophagy in the liver and heart of newborn rats. The effects of glucagon, adrenalin or rapamycin
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DOI:
10.14670/hh-20.689
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发表时间:
2005-07-01
影响因子:
2
通讯作者:
Hann, AC
Hann, AC
中科院分区:
生物学4区
文献类型:
--
作者:
Kondomerkos, DJ;Kalamidas, SA;Hann, AC

文献摘要

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采用生化法和电镜法研究了胰高血糖素、肾上腺素和雷帕霉素对新生大鼠肝脏和心脏糖原自噬的影响。胰高血糖素或肾上腺素增加了肝细胞和心肌细胞的自噬活性、肝和心脏的糖原水解酸葡萄糖苷酶活性以及自噬空泡内糖原的降解。胰高血糖素或肾上腺素也会增加肝脏中麦芽糖水解酸葡萄糖苷酶的活性,但不会增加心脏中的活性。雷帕霉素在新生儿心脏中也产生了类似的效果。这些观察结果支持了先前的研究,即控制新生动物肝脏和心脏糖原自噬的细胞机制是由环AMP和mTOR途径调节的。
The effects of glucagon, adrenalin or rapamycin on glycogen autophagy in the liver and heart of newborn rats were studied using biochemical determinations and electron microscopy. Glucagon or adrenalin increased autophagic activity in the hepatocytes and myocardiocytes, glycogen-hydrolyzing acid glucosidase activity in the liver and heart and degradation of glycogen inside the autophagic vacuoles. Glucagon or adrenalin also increased the maltose-hydrolyzing acid glucosidase activity in the liver, but not in the heart. Similar effects were produced in the newborn heart by rapamycin.These observations support previous studies suggesting that the cellular machinery which controls glycogen autophagy in the liver and heart of newborn animals, is regulated by the cyclic AMP and the mTOR pathways.