Flaxseed Oil Attenuates Nonalcoholic Fatty Liver of Hyperlipidemic Hamsters
Flaxseed Oil Attenuates Nonalcoholic Fatty Liver of Hyperlipidemic Hamsters
Year: 2009
Authors: Yang, S.-F. Tseng, J.-K. Chang, Y.-Y. Chen, Y.-C.
Publication Name: J. Agric. Food Chem.
Publication Details: Volume 57; Pages 5078 – 5083.
Abstract:
Hyperlipidemia of hamsters was induced by high-fat/cholesterol diets formulated by the addition of coconut oil (CO), butter (BU), and flaxseed oil (FX). Lower (p < 0.05) serum lipids, liver size, and hepatic cholesterol and triacylglycerol contents were observed in the FX group compared to both CO and BU groups. The liver damage indices [glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) values] in the FX group were lower (p < 0.05) than those in the CO and BU groups, which may result from higher (p < 0.05) glutathione (GSH) levels and a tendency toward lower malondialdehyde (MDA) levels in livers. Besides, lower (p < 0.05) gene expression and activity of hepatic matrix metalloproteinases-9 (MMP-9) in the FX group were lower (p > 0.05) compared to those in the CO and BU groups; however, no ( p > 0.05) differences in gene expression activities of hepatic MMP-2 were observed among treatments. Those beneficial effects could explain the attenuation of FX on nonalcoholic fatty liver (NAFL) induced by a high-fat/ cholesterol dietary habit. (Authors abstract)
Nonalcoholic fatty liver (NAFL) is linked to obesity, diabetes, and hyperlipidemia. High-fat diets result in high body weights, serum lipids, and hepatic lipids in the form of triacylglycerol. NAFL also causes a chronic inflammation and may be associated with progression to the end-stage of liver disease. Liver fibrosis is caused by recurrent wound healing in response to various sources of chronic liver damage, for example, hepatic fat deposition and peroxidatin which cause chronic inflammation and extracellular matrix (ECM) remodeling. Major components of the ECM in liver fibrosis are collagen types I, III, and IV. Matrix metalloproteinases (MMPs), MMP-1, -2, and -9, play a central role in degradations of these collagens, resulting in ECM remolding. Increased MMP-2 and -9 gene expressions or activities are regarded as major causes of liver fibrosis. No studies regarding the hepatoprotection of flaxseed on NAFL by a high-fat/cholesterol-diet have been reported. Thus the objectives of the present study were to investigate if the occurrence of nonalcoholic fatty liver attenuated by FX supplementation in hyperlipidemic hamsters is via (1) decreasing liver lipid accumulation, (2) lowering liver lipid peroxidation or increasing antioxidant capacity, or (3) reducing hepatic MMP-2 and -9 gene expressions and activities. The data demonstrate that body weight gain and liver size were decreased upon high-fat/cholesterol diets with FX. FX reduced serum TC and TAG compared to the other high-fat/cholesterol dietary diets (BU and CO groups). The FX diet did not reduce serum TC or TAG to the levels of the control diet. Decreased hepatic cholesterol concentration in the FX group was observed. A higher fecal lipid excretion related to lower serum lipid level was also reported. The authors assumed that the lowering effects of FX on serum and hepatic lipids are highly associated with higher fecal lipid outputs and hepatic lipid expenditure, as well as less hepatic lipid accumulation. In the present study, a tendency toward lower MDA contents (a prooxidant) in the FX and control groups compared to those in the CO and BU groups may be associated with lower hepatic cholesterol and triacylglycerol levels in the FX and control groups, which may decrease the depletion of hepatic GSH contents (an antioxidant). The authors also speculated that consumption of FX is capable of increasing the concentration of n-3 PUFAs in the body, which could modulate inflammation by inactivation of cytokines, thus reducing gene expressions and activities of MMP-9. FX also decreases the hepatic lipid accumulation and hepatic GSH depletion induced by a high-fat/cholesterol diet. These benefits of FX further minimize liver damage in a high-fat/cholesterol diet. In summary, the results demonstrate that FX markedly attenuates NAFL of hyperlipidemic hamsters. The attenuation of liver damage was associated with lower hepatic cholesterol and triacylglycerol levels, GSH depletion, and hepatic MMP-9 gene expressions and activities. On the basis of those beneficial effects, FX may attenuate the NAFL induced by the consumption of a high-fat/cholesterol habit. (Editors comments)
Nonalcoholic fatty liver (NAFL) is linked to obesity, diabetes, and hyperlipidemia. High-fat diets result in high body weights, serum lipids, and hepatic lipids in the form of triacylglycerol. NAFL also causes a chronic inflammation and may be associated with progression to the end-stage of liver disease. Liver fibrosis is caused by recurrent wound healing in response to various sources of chronic liver damage, for example, hepatic fat deposition and peroxidatin which cause chronic inflammation and extracellular matrix (ECM) remodeling. Major components of the ECM in liver fibrosis are collagen types I, III, and IV. Matrix metalloproteinases (MMPs), MMP-1, -2, and -9, play a central role in degradations of these collagens, resulting in ECM remolding. Increased MMP-2 and -9 gene expressions or activities are regarded as major causes of liver fibrosis. No studies regarding the hepatoprotection of flaxseed on NAFL by a high-fat/cholesterol-diet have been reported. Thus the objectives of the present study were to investigate if the occurrence of nonalcoholic fatty liver attenuated by FX supplementation in hyperlipidemic hamsters is via (1) decreasing liver lipid accumulation, (2) lowering liver lipid peroxidation or increasing antioxidant capacity, or (3) reducing hepatic MMP-2 and -9 gene expressions and activities. The data demonstrate that body weight gain and liver size were decreased upon high-fat/cholesterol diets with FX. FX reduced serum TC and TAG compared to the other high-fat/cholesterol dietary diets (BU and CO groups). The FX diet did not reduce serum TC or TAG to the levels of the control diet. Decreased hepatic cholesterol concentration in the FX group was observed. A higher fecal lipid excretion related to lower serum lipid level was also reported. The authors assumed that the lowering effects of FX on serum and hepatic lipids are highly associated with higher fecal lipid outputs and hepatic lipid expenditure, as well as less hepatic lipid accumulation. In the present study, a tendency toward lower MDA contents (a prooxidant) in the FX and control groups compared to those in the CO and BU groups may be associated with lower hepatic cholesterol and triacylglycerol levels in the FX and control groups, which may decrease the depletion of hepatic GSH contents (an antioxidant). The authors also speculated that consumption of FX is capable of increasing the concentration of n-3 PUFAs in the body, which could modulate inflammation by inactivation of cytokines, thus reducing gene expressions and activities of MMP-9. FX also decreases the hepatic lipid accumulation and hepatic GSH depletion induced by a high-fat/cholesterol diet. These benefits of FX further minimize liver damage in a high-fat/cholesterol diet. In summary, the results demonstrate that FX markedly attenuates NAFL of hyperlipidemic hamsters. The attenuation of liver damage was associated with lower hepatic cholesterol and triacylglycerol levels, GSH depletion, and hepatic MMP-9 gene expressions and activities. On the basis of those beneficial effects, FX may attenuate the NAFL induced by the consumption of a high-fat/cholesterol habit. (Editors comments)
