The remnant liver tissues of the adult male rats after partial hepatectomy by the method of HIGGINS and ANDERSON were studied by electron microscopy, Particular attention was paid to the mechanism of the formation of fatty liver from the viewpoint of morphology.
During first ten hours after partial hepatectomy, the hepatic parenchymal cells showed various degenerating processes in the cytoplasm. Mitochondria were swollen and often deformed. Glycogen particles were remarkably reduced and at last disappeared from the cytoplasmic matrix, whereas agranular endoplasmic reticulum was increased to develope. There appeared to be some intimate reciprocal relationships between the depletion of glycogen and the increase of agranular endoplasmic reticulum. At this stage, however, no lipid particles appeared in the cytoplasm.
Fifteen hours after hepatectomy, glycogen particles disappeared completely from the cytoplasm. Instead, lipid droplets began to deposit in the cytoplasmic matrix in close association with agranular endoplasmic reticula.
On the other hand, the cytoplasm close to the space of DISSE showed the prominent increase of pinocytotic vesicles, the cavity of which contained small dense particles, presumably mobilized fat particles. Similar dense particles were also observed confined to agranular vesicles in the cytoplasm apart from the cell surface, where dense particles tended to develope into large droplets by coalescence, and at last to lose their limiting membranes. All of these were assumed to represent the process linked with each other, to which lipid depositions are at least in part attributed.
Twenty hours after hepatectomy, the maximum deposition of lipid in the cytoplasm was observed and the peripheral region of cytoplasm contained much more lipid than the central. Most parts of the cytoplasm were occupied with well-developed agranular endoplasmic reticulum.
Two days after operation, or thereafter, glycogen particles again began to appear in the cytoplasm. Instead, at the same time, the lipid droplets were gradually decreased and finally disappeared from the cytoplasm.
Five to ten days after operation, the parenchymal cells did not show any changes in fine structure but returned to the appearance of normal cells.
From the present study, it is assumed that in the remnant hepatic parenchymal cells after partial hepatectomy, glycogen particles are promptly consumed for increased need of energy supply owing to high metabolic rate, and that, in following the depletion of glycogen, fats are mobilized as energy source to the liver from peripheral depots.
The present study suggests the possibility that the fatty liver after partial hepatectomy is in part induced by the metabolic transformation from glycogen to lipids, and in part by the mobilization of lipids to the liver from the peripheral depots. It is in any way apparent that formation of glycogen and fat occurs in close association with agranular endoplasmic reticulum.
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