Different Dietary Proportions of Fish Oil Regulate Inflammatory Factors but Do Not Change Intestinal Tight Junction ZO-1 Expression in Ethanol-Fed Rats.

Yi-Wen Chien,Suh-Ching Yang,Hsiao-Yun Wang,Hsiao-Li Chuang,Man-Hui Pai,Ya-Ling Chen,Hsiang-Chi Peng

doi:10.1155/2017/5801768

Abstract

Sixty male Wistar rats were fed a control or an ethanol-containing diet in groups C or E. The fat compositions were adjusted with 25% or 57% fish oil substituted for olive oil in groups CF25, CF57, EF25, and EF57. Hepatic thiobarbituric acid-reactive substance (TBARS) levels, cytochrome P450 2E1 protein expression, and tumor necrosis factor- (TNF-) α, interleukin- (IL-) 1β, IL-6, and IL-10 levels, as well as intracellular adhesion molecule (ICAM)-1 levels were significantly elevated, whereas plasma adiponectin level was significantly reduced in group E (p < 0.05). Hepatic histopathological scores of fatty change and inflammation, in group E were significantly higher than those of group C (p < 0.05). Hepatic TBARS, plasma ICAM-1, and hepatic TNF-α, IL-1β, and IL-10 levels were significantly lower, and plasma adiponectin levels were significantly higher in groups EF25 and EF57 than those in group E (p < 0.05). The immunoreactive area of the intestinal tight junction protein, ZO-1, showed no change between groups C and E. Only group CF57 displayed a significantly higher ZO-1 immunoreactive area compared to group C (p = 0.0415). 25% or 57% fish oil substituted for dietary olive oil could prevent ethanol-induced liver damage in rats, but the mechanism might not be related to intestinal tight junction ZO-1 expression.

Highlights

Excessive or chronic alcohol consumption can lead to liver damage through various pathogenic mechanisms
Rats were fed with either a control diet or ethanol diet, in which the fat composition of both diets was adjusted with 25% (7.1 g fish oil/kg diet, 6% of total calories) or 57% (16.2 g fish oil/kg diet, 15% of total calories) fish oil substituted for olive oil
No difference was found in food intake among the six groups

Summary

Introduction

Excessive or chronic alcohol consumption can lead to liver damage through various pathogenic mechanisms. Three primary types of alcohol-induced liver damage include fatty liver, hepatitis, and cirrhosis [1]. Alcohol-induced liver damage is related to an increased NADH/NAD+ ratio which promotes fatty acid synthesis and lipid accumulation in liver cells, oxidative stress caused by increased CYP2E1 activity, and an increased endotoxin level which triggers Kupffer’s cell activation and inflammatory processes [2,3,4]. It was indicated that higher endotoxin levels were observed in alcoholic liver disease (ALD) patients, and gut leakage seemed to be the main cause [6, 7].

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