2006•PubMedRequires access
[Liver regenerative capacity after partial hepatectomy in rats with nonalcoholic fatty liver disease].
Xue-feng Dai, Dongfeng Chen
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Abstract
OBJECTIVE: To explore the changes of liver regeneration after partial hepatectomy on rats with nonalcoholic fatty liver disease (NAFLD) caused by a high fat diet. METHODS: One hundred Wistar rats were randomly divided into a control group (group C, n = 45), fed with normal diet, and a NAFLD group, fed with fat-rich diet (group F, n = 55). All rats had a 70% partial hepatectomy at the end of the 12th week. They were sacrificed at postoperative 0, 1, 12, 24, or 36 hours and the percentages of their regenerated liver masses were calculated. The mitosis index was measured microscopically and the changes of cell ultrastructure were observed under an electron microscope. The expression of proliferating cell nuclear antigen (PCNA) was detected using immunohistochemistry. The expression of mRNA of cyclin D1 was measured by RT-PCR. RESULTS: The light and electron microscopy showed that the hepatic sinusoids expanded at an early period after the partial hepatectomy. The mitochondria and rough endoplasmic reticulum (RER) expanded and their number increased. The mitosis index was increased. The sinusoids of the livers in group F were narrow and irregular. The nuclei were smaller and the necrotic cells increased. As compared with the control group, the mitosis index was significantly decreased (P < 0.01), and the regenerative liver weight ratio in group F was lower at postoperative 12 h, 24 h, 36 h (P < 0.01). PCNA labeling index in group F also was lower than that in group C. The peak of the PCNA in group F was later than that of the control group (P < 0.01). In group C, the mRNA of cyclin D1 peaked at the 24th hour after the partial hepatectomy, and then decreased afterwards. In group F, it was lower than that of group C at the same time (P < 0.01). CONCLUSION: After NAFLD rats had partial hepatectomies, the capacity of their liver regeneration decreased and the peak of DNA synthesis was delayed, and at the same time the morbidity of the rats increased.