糖原
胰高血糖素
自噬
内科学
内分泌学
肾上腺素
糖原分解
液泡
生物
化学
胰岛素
生物化学
医学
细胞质
细胞凋亡
作者
Dimitrios J. Kondomerkos,Stefanos A. Kalamidas,O.B. Kotoulas,A.C. Hann
出处
期刊:PubMed
[National Institutes of Health]
日期:2005-07-01
卷期号:20 (3): 689-96
被引量:58
摘要
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.
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