An electron microscopic and biochemical study of the effects of propranolol on the glycogen autophagy in newborn rat hepatocytes

• Published in: Histology and histopathology Vol. 18; no. 3; p. 811
• Main Authors: Kotoulas, O B, Kalamidas, S A, Miles, P, Hann, A C
• Format: Journal Article
• Language: English
• Published: Spain 01.07.2003
• Subjects: Adenosine Triphosphatases - metabolism; Adrenergic beta-Antagonists - pharmacology; alpha-Glucosidases - metabolism; Animals; Animals, Newborn; Autophagy; Biochemical Phenomena; Biochemistry; Cells, Cultured; Cyclic AMP - metabolism; Cyclic AMP-Dependent Protein Kinases - metabolism; Glycogen - metabolism; Hepatocytes - metabolism; Immunohistochemistry; Liver - metabolism; Microscopy, Electron; Phosphoric Monoester Hydrolases - metabolism; Propranolol - pharmacology; Rats; Time Factors
• ISSN: 0213-3911
• DOI: 10.14670/HH-18.811

The effects of propranolol on the glycogen autophagy in newborn rat hepatocytes were studied by using biochemical determinations, electron microscopy and morphometric analysis. Propranolol lowered the liver cyclic AMP and cyclic AMP-dependent protein kinase activity. It also decreased the formyl-methionyl-leucyl-phenylalanine (FMLP)-inhibitable Ca2+-ATPase activity including lysosomal calcium uptake pump. The normal postnatal increase in the volume of autophagic vacuoles and the activity of acid glycogen-hydrolyzing alpha glucosidase were inhibited. Also, the degradation of glycogen inside the autophagic vacuoles was apparently inhibited. The activity of acid mannose 6-phosphatase was increased. These findings indicate that propranolol influences several steps in the sequence of events leading to the breakdown of glycogen in the autophagic vacuoles of newborn rat hepatocytes. This supports our previous studies suggesting that cyclic AMP regulates glycogen autophagy.