Kondomerkos D J, Kalamidas S A, Kotoulas O B, Hann A C
Department of Anatomy, Histology and Embryology, Medical School, University of Ioannina, 45110 Ioannina, Greece.
Histol Histopathol. 2005 Jul;20(3):689-96. doi: 10.14670/HH-20.689.
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.
采用生化测定和电子显微镜技术,研究了胰高血糖素、肾上腺素或雷帕霉素对新生大鼠肝脏和心脏中糖原自噬的影响。胰高血糖素或肾上腺素增加了肝细胞和心肌细胞中的自噬活性、肝脏和心脏中糖原水解酸性葡萄糖苷酶的活性以及自噬泡内糖原的降解。胰高血糖素或肾上腺素还增加了肝脏中麦芽糖水解酸性葡萄糖苷酶的活性,但在心脏中未增加。雷帕霉素在新生心脏中产生了类似的效果。这些观察结果支持了先前的研究,表明控制新生动物肝脏和心脏中糖原自噬的细胞机制受环磷酸腺苷和mTOR信号通路的调节。