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Nutr Hosp. 2018 Feb 16;35(2):318-325. doi: 10.20960/nh.1294.

Açai improves non-alcoholic fatty liver disease (NAFLD) induced by fructose.

Author information

1
Federal University of Ouro Preto, Ouro Preto, MG, Brazil. mlpedrosa@gmail.com.

Abstract

INTRODUCTION:

the excessive consumption of fructose can cause liver damage, characteristic of non-alcoholic fatty liver disease (NAFLD) associated with changes in lipid metabolism and antioxidant defenses. Açai, the fruit of Euterpe oleraceaMart., has demonstrated numerous biological activities, including anti-inflammatory, antioxidant, and lipid metabolism modulating action.

OBJECTIVE:

we evaluated the benefits of açai supplementation on liver damage caused by replacing starch with fructose in rats.

METHODS:

thirty male Fischerrats were divided into two groups, the control group (C, 10 animals), which consumed a standard diet (AIN-93M), and the fructose (F, 20 animals) group, which consumed a diet containing 60% of fructose. After eight weeks, 10 animals from the fructose group received 2% of lyophilized açai, and were called the açai fructose group (FA). The animals were fed ad libitumwith these diets for another ten weeks. Serum, hepatic and fecal lipid profile, antioxidant enzymes and carbonylated protein were assessed and histopathological characterization of the liver was performed.

RESULTS:

açai promoted the reduction of ALT activity in relation to the fructose group (F), reduced alkaline phosphatase to a level similar to that of the control group (C) in relation to the fructose group (F), and reduced catalase activity. The fruit also increased the ratio of total/oxidized glutathione (GSH/GSSG) and reduced the degree of macrovesicular steatosis and the number of inflammatory cells.

CONCLUSION:

the replacement of starch by fructose during this period was effective in promoting NAFLD. Açai showed attenuating effects on some markers of hepatic steatosis and inflammation.

PMID:
29756964
DOI:
10.20960/nh.1294
[Indexed for MEDLINE]
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