Reconstitution of liver mass via cellular hypertrophy in the rat

The liver has an extremely effective regenerative capacity. When 70% of a r at liver is removed by surgery, the liver mass regrows in 7 to 10 days by t he compensatory hyperplasia of the remnant part. In case of damage to the s urviving hepatocytes, the facultative stem-cell compartment is activated an d the liver regenerates by means of oval-cell proliferation/differentiation . In the present study, we demonstrate that when both hepatocyte proliferat ion and stem-cell activation were prevented by dexamethasone (Dex) administ ration, the liver mass was restored in the absence of DNA synthesis. The re storation of the liver was accomplished by the preferential enlargement/hyp ertrophy of the periportal hepatocytes. A similar response was observed whe n cell proliferation was arrested by S-fluorouracil (FU) following partial hepatectomy. Therefore, the hepatocytic hypertrophy appears to provide an a lternative mechanism of liver-mass restoration. This hypertrophic condition of the liver is not stable, because following the withdrawal of Dex, the e nlarged hepatocytes entered in the cell cycle and the normal liver structur e and DNA content was re-established.