A Combination of Flaxseed Oil and Astaxanthin Improves Hepatic Lipid Accumulation and Reduces Oxidative Stress in High Fat-Diet Fed Rats.

Key Findings:

Non alcoholic fatty liver disease (NAFLD), which includes benign hepatic steatosis and cirrhosis, has been shown to be associated with obesity, hyperlipidemia and type II diabetes.  ALA can compete with linoleic acid to reduce arachidonic acid or act as a precursor for longer chain n-3 PUFAs (such as EPA and DHA), or it can directly interact with nuclear receptors and ion channels to produce positive effects.  Astaxanthin (ASX) has been shown to protect against hepatic endoplasmic reticular stress, inflammation and lipid deposition in high fat, high-fructose fed mice [16,17], as well as protect against dioxin-induced hepatotoxicity. Here a combination of ALA and ASX was studied for effects on reducing liver damage in rats fed a high-fat diet.  The results showed that FO plus ASX can reduce hepatic steatosis, TG, cholesterol and oxidative stress, suggesting that this may reduce NAFLD induced by a high-fat diet. Thus, FO + ASX may be promising for hepatoprotection.

ABSTRACT

Hepatic lipid accumulation and oxidative stress are crucial pathophysiological mechanisms for non-alcoholic fatty liver disease (NAFLD). Thus, we examined the effect of a combination of flaxseed oil (FO) and astaxanthin (ASX) on hepatic lipid accumulation and oxidative stress in rats fed a high-fat diet. ASX was dissolved in flaxseed oil (1 g/kg; FO + ASX). Animals were fed diets containing 20% fat, where the source was lard, or 75% lard and 25% FO + ASX, or 50% lard and 50% FO + ASX, or FO + ASX, for 10 weeks. Substitution of lard with FO + ASX reduced steatosis and reduced hepatic triacylglycerol and cholesterol. The combination of FO and ASX significantly decreased hepatic sterol regulatory element-binding transcription factor 1 and 3-hydroxy-3-methylglutaryl-CoA reductase but increased peroxisome proliferator activated receptor expression. FO + ASX significantly suppressed fatty acid synthase and acetyl CoA carboxylase but induced carnitine palmitoyl transferase-1 and acyl CoA oxidase expression. FO + ASX also significantly elevated hepatic SOD, CAT and GPx activity and GSH, and markedly reduced hepatic lipid peroxidation. Thus, FO and ASX may reduce NAFLD by reversing hepatic steatosis and reducing lipid accumulation and oxidative stress.