Abstract
Background and AimThe progression of non-alcoholic fatty liver disease (NAFLD) likely involves a ‘multiple hit’ mechanism. We hypothesized that partial hepatectomy, a procedure performed frequently in patients with NAFLD, would accelerate the progression of disease.MethodsC57BL/6JolaHsd mice were fed a choline-deficient L-amino acid-defined diet (CD-AA) or a choline-sufficient L-amino acid-defined control diet (CS-AA). Part of the mice in the CD-AA group received a diet enriched in vitamin E (~20 mg /day). Two weeks after the start of the diet, mice underwent a partial hepatectomy or a sham operation.ResultsIn the CD-AA group, NAFLD activity scores were significantly higher at 7 days after partial hepatectomy compared to the sham operated mice (3.7 ± 1.3 vs. 1.8 ± 0.7; P<0.05). In addition, TBARS, a measure for oxidative stress, in liver tissue of the CD-AA group were significantly higher at day 1, 3 and 7 after partial hepatectomy compared to the sham operated mice (P<0.05). Vitamin E therapy significantly reduced TBARS level at day 7 after partial hepatectomy compared to the CD-AA diet group (P< 0.05). Vitamin E suppletion reduced NAFLD activity score at day 7 after partial hepatectomy compared to the CD-AA group (2.3 ± 0.8 vs. 3.8 ± 1.0; P<0.05).ConclusionPartial hepatectomy accelerates the progression of NAFLD. Disease progression induced by partial hepatectomy is substantially attenuated by vitamin E.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver disorders worldwide [1]
In the choline-deficient L-amino acid-defined diet (CD-AA) group, non-alcoholic fatty liver disease (NAFLD) activity scores were significantly higher at 7 days after partial hepatectomy compared to the sham operated mice (3.7 ± 1.3 vs. 1.8 ± 0.7; P
Thiobarbituric acid-reactive substances (TBARS), a measure for oxidative stress, in liver tissue of the CD-AA group were significantly higher at day 1, 3 and 7 after partial hepatectomy compared to the sham operated mice (P
Summary
Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver disorders worldwide [1]. NAFLD includes a disease spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), which may eventually progress to liver fibrosis and cirrhosis [2]. Mechanisms of disease progression in NAFLD are incompletely understood, but likely a “multiple-hit” model is involved [2]. In this model, the development of steatosis increases the sensitivity of the liver to other hits such as oxidative stress and cytokines, leading to hepatocyte damage and liver dysfunction [3,4]. The progression of non-alcoholic fatty liver disease (NAFLD) likely involves a ‘multiple hit’ mechanism. We hypothesized that partial hepatectomy, a procedure performed frequently in patients with NAFLD, would accelerate the progression of disease
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