Summary
The left part of median lobe of rat liver (10–15% of total liver weight) was separated from the portal blood flow by ligation of the branch of the portal vein. Adult male rats were operated in the morning (the time of maximal liver glycogen content). After 2–5 hrs one observes in acinoperipheral liver cells a large quantity of autophagic vacuoles containing cytoplasmic organelles and/or glycogen. Such vacuoles often show acid phosphatase activity. The segregation of glycogen is a partial phenomenon of the enhanced cellular autophagy observed under the experimental conditions. It depends on a sufficient glycogen content of the cell at the time of the insult but other studies have shown that glycogen reserves are not prerequisite. Intravacuolar glycogen does not indicate a pathological or specific reaction of the liver cell since glycogen is segregated in a small rate under physiological conditions. In general, accumulation of glycogen within vacuoles may be the result 1. of an enhanced cellular autophagy, as in our and other experiments or 2. of an enzyme deficiency blocking the hydrolytic breakdown of the physiologically segregated glycogen, as in glycogenosis type II (Pompes disease). Segregated glycogen is observed under the experimental conditions also within tubular or vesicular formations. Such structures extend the morphological spectrum of cellular autophagy.
Zusammenfassung
Bei ausgewachsenen Ratten wird durch Unterbindung eines kleinen Pfortaderastes die linke Hälfte des mittleren Leberlappens (10–15% der Leber) aus der portalen Zirkulation ausgeschaltet. In den ersten Stunden danach beobachtet man in läppchenperipheren Epithelien des portalischämischen Gewebes zahlreiche autophagische Vacuolen, die in wechselndem Ausmaße, und nicht selten ausschließlich Glykogen enthalten. Sie können bei der Reaktion auf saure Phosphatase fermentpositiv sein. Die Glykogensegregation im Rahmen einer gesteigerten cellulären Autophagie hat einen hinreichenden Glykogengehalt der Zelle zum Zeitpunkt des Insultes zur Voraussetzung. Sie ist keine spezifische Reaktion auf bestimmte Noxen, da Glykogen in geringem Umfange schon physiologischerweise segregiert wird. Generell gibt es zwei Ursachen für eine Anhäufung von Glykogen in Vacuolen: 1. eine gesteigerte celluläre Autophagie, wie in den eigenen und anderen Untersuchungen; 2. eine Störung im hydrolytischen Abbau des unter Normalbedingungen segregierten Glykogens, wie bei der Glykogenose Typ II. Segregiertes Glykogen kommt unter den Versuchsbedingungen auch innerhalb tubulo-vesiculärer Formationen vor, die das morphologische Spektrum der cellulären Autophagie erweitern.
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Pfeifer, U. Celluläre Autophagie: Glykogensegregation im Frühstadium einer partiellen Leberatrophie. Virchows Arch. Abt. B Zellpath. 5, 242–253 (1970). https://doi.org/10.1007/BF02893566
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DOI: https://doi.org/10.1007/BF02893566