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Updated: Jun 14, 2026

Partial Lobular Hepatectomy: A Surgical Model for Morphologic Liver Regeneration
Published on: May 31, 2018
Effect of S-adenosylmethionine on liver regeneration induced by partial hepatectomy
Lukás Kohoutek1, Zuzana Cervinková, Otto Kucera
1Department of Physiology, Faculty of Medicine, Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic.
Abstract:
S-adenosylmethionine (SAMe) is a key metabolite regulating growth, differentiation and death of hepatocytes. Experimentally, exogenous SAMe has been documented to attenuate hepatocarcinogenesis. The aim of our study was to evaluate the effect of SAMe on proliferation of hepatocytes that are not cancerously transformed. Partial 2/3 hepatectomy (PH) was performed in rats, control animals underwent laparotomy. SAMe was injected immediately after the surgery and then at 24 h intervals for two days at 10 or 40 mg/kg. The animals were sacrificed 24, 48 and 72 h after operation and the intensity of liver regeneration was evaluated. SAMe treatment at 10 mg/kg was associated with decrease in the synthesis of liver DNA 48 h after PH, however, it was not reflected in DNA content. SAMe treatment at 40 mg/kg led to the reduction of DNA synthesis 72 h after PH followed by the diminution of DNA content. The results have documented the inhibition of the liver regeneration by SAMe that may be mediated by the suppression of liver fat accumulation. Cell GSH level correlating with the growth rate was not affected by SAMe. Prevention from the decrease in the intracellular content of SAMe, as a factor attenuating regeneration remains to be verified.
Insights
S-adenosylmethionine (SAMe) inhibits liver regeneration in rats after partial hepatectomy. This effect may involve suppressing fat accumulation, but further research is needed to confirm SAMe
Area of Science:
- Hepatology
- Biochemistry
- Regenerative Medicine
Background:
- S-adenosylmethionine (SAMe) is a crucial metabolite regulating hepatocyte functions.
- Exogenous SAMe has shown potential in attenuating hepatocarcinogenesis.
Purpose of the Study:
- To investigate the effect of SAMe on the proliferation of non-cancerous hepatocytes.
- To evaluate SAMe's impact on liver regeneration following partial hepatectomy.
Main Methods:
- Partial 2/3 hepatectomy (PH) was performed in rats.
- SAMe was administered at doses of 10 mg/kg or 40 mg/kg post-surgery.
- Liver regeneration was assessed by measuring DNA synthesis and content at various time points.
Main Results:
- SAMe treatment (10 mg/kg) decreased liver DNA synthesis at 48 hours post-PH.
- Higher SAMe dose (40 mg/kg) reduced DNA synthesis and content at 72 hours post-PH.
- SAMe inhibited liver regeneration, potentially by suppressing fat accumulation; GSH levels remained unaffected.
Conclusions:
- SAMe demonstrates an inhibitory effect on liver regeneration post-hepatectomy.
- The mechanism may involve the suppression of hepatic fat accumulation.
- Further studies are required to verify if preventing intracellular SAMe depletion can attenuate regeneration.

