Omega-3 fatty acids reduce hepatic steatosis and consequently attenuate ischemia-reperfusion injury following partial hepatectomy in rats

Abstract Aim The aim of this study was to investigate omega-3 fatty acids (FAs) treatment of experimental steatosis and the consequent effect on ischemia-reperfusion (IR) injury. Background Fatty livers are more susceptible to IR injury and display decreased regenerative capacity. Consequently, rest...

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Published inDigestive and liver disease Vol. 43; no. 12; pp. 984 - 990
Main Authors Marsman, Hendrik A, Heger, Michal, Kloek, Jaap J, Nienhuis, Syert L, ten Kate, Fiebo J.W, van Gulik, Thomas M
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Ltd 01.12.2011
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Summary:Abstract Aim The aim of this study was to investigate omega-3 fatty acids (FAs) treatment of experimental steatosis and the consequent effect on ischemia-reperfusion (IR) injury. Background Fatty livers are more susceptible to IR injury and display decreased regenerative capacity. Consequently, restrictions exist for patients with fatty livers to undergo a major hepatectomy or to participate in living donor liver transplantation. Until recently, weight reduction constituted the only proven therapy for patients with fatty livers. Methods Steatosis was induced by a 3-wk methionine/choline-deficient diet, followed by oral administration of omega-3 FAs (Omega-3), standard lipid solution (Lipid), or NaCl (Saline) during 2 wk. Control animals received a standard diet without treatment. Rats underwent partial (70%) hepatic IR combined with partial hepatectomy (PHx) of the non-ischemic lobes (30%) followed by 24-h reperfusion. Results Histological analysis revealed mild (5–33%) macrovesicular steatosis in omega-3-treated animals vs. severe (>66%) macrovesicular steatosis in both Lipid and Saline groups. Following IR/PHx, omega-3-treated rats exhibited reduced serum ALT levels after 6- and 24-h reperfusion, a reduced hepatic TNF-α content, and an improved anti-oxidative capacity. Conclusions Omega-3 treatment significantly reduces experimental hepatic steatosis and associated pathophysiological features, resulting in significantly reduced IR injury following PHx.
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ISSN:1590-8658
1878-3562
DOI:10.1016/j.dld.2011.07.009