Omega-3s Protects Against Nonalcoholic Fatty Liver Disease & Blocks Omega-6 Fat Compounds
Bottomline: Omega-3 fatty acids protected the liver from damage, triggered by obesity and insulin resistance. Omega-3s blocked inflammatory compounds derived from the omega-6 fatty acid, arachidonic acid; while creating liver-protecting compounds, called resolvins and protectins.
FASEBJ February 11, 2009.
Background: Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease, which can ultimately lead to liver failure. This condition is triggered by metabolic syndrome (obesity and insulin resistance), which results in the accumulation of fat in the liver, which creates inflammation and scarring (cirrhosis).
While the omega-3 fatty acids, DHA and EPA, are well known for their anti-inflammatory properties, scientists recently discovered that they generate potent bioactive mediators, called Resolvins and protectins, which have profound protective properties. Since obesity is characterized as a low grade inflammatory state, and fat cells secrete compounds which modulate both inflammation and insulin; researchers wanted to explore the impact of omega-3 fats on this condition.
Summary: Scientists evaluated whether omega-3-polyunsaturated fatty acids can alter the function of adipose tissue, while protecting the liver from insulin resistance and the accumulation of fat. They also elucidated possible mechanisms of action.
Genetically altered mice (prone to obesity, insulin resistance and fatty liver disease) were divided into four groups. One group was given an omega-3-enriched diet and the second group was given a control diet for a five week period. The third group was injected with the omega-3 fatty acid (DHA), and the fourth group received an injection of the omega-3 fatty acid-derived compound, resolvin. Blood and tissue samples were evaluated.
The omega-3-rich diet improved insulin tolerance and decreased inflammation. The key mechanisms by which the omega-3s exerted their beneficial impact included:
Conclusion: These findings, together with evidence from other studies, provide a strong rationale for omega-3 supplementation for patients with liver disease.
Study Quote:"One of the most important findings of our study was that increased intake of omega-3-polyunsaturated fatty acids inhibited the formation of eicosanoids derived from the omega-6-polyunsaturated fatty acids arachidonic acid."
Links:
Ana González-Périz, Raquel Horrillo, Natàlia Ferré, Karsten Gronert, Baiyan Dong, Eva Morán-Salvador, Esther Titos, Marcos Martínez-Clemente, Marta López-Parra, Vicente Arroyo, and Joan Clària.Obesity-induced insulin resistance and hepatic steatosis are alleviated by
-3 fatty acids: a role for resolvins and protectins .FASEBJ Express 10.1096/fj.fj.08-125674, published online February 11, 2009.
Further Reading (Full Text Sources):
Hasturk H et al. ,
Resolvin E1 Regulates Inflammation at the Cellular and Tissue Level and Restores Tissue Homeostasis In Vivo. J Immunol 2007 179: 7021-7029
Serhan CN et al.
Resolution of inflammation: state of the art, definitions and terms FASEB J. (2007)21: 325-332.
FASEBJ February 11, 2009.
Background: Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease, which can ultimately lead to liver failure. This condition is triggered by metabolic syndrome (obesity and insulin resistance), which results in the accumulation of fat in the liver, which creates inflammation and scarring (cirrhosis).
While the omega-3 fatty acids, DHA and EPA, are well known for their anti-inflammatory properties, scientists recently discovered that they generate potent bioactive mediators, called Resolvins and protectins, which have profound protective properties. Since obesity is characterized as a low grade inflammatory state, and fat cells secrete compounds which modulate both inflammation and insulin; researchers wanted to explore the impact of omega-3 fats on this condition.
Summary: Scientists evaluated whether omega-3-polyunsaturated fatty acids can alter the function of adipose tissue, while protecting the liver from insulin resistance and the accumulation of fat. They also elucidated possible mechanisms of action.
Genetically altered mice (prone to obesity, insulin resistance and fatty liver disease) were divided into four groups. One group was given an omega-3-enriched diet and the second group was given a control diet for a five week period. The third group was injected with the omega-3 fatty acid (DHA), and the fourth group received an injection of the omega-3 fatty acid-derived compound, resolvin. Blood and tissue samples were evaluated.
The omega-3-rich diet improved insulin tolerance and decreased inflammation. The key mechanisms by which the omega-3s exerted their beneficial impact included:
• Up-regulating the genes involved in: insulin sensitivity, glucose transport and insulin receptor signaling.Together the actions of omega-3 fats attenuated fatty liver, (hepatic steatosis).
• Increasing adiponectin, the anti-inflammatory compound produced by fat cells, which also improves insulin sensitivity.
• Creating protectins and resolvins, which offered a level of protection similar to that of rosiglitazone, a medication used to treat diabetes.
• Blocking the formation of potent inflammatory compounds made from the omega-6 fatty acid, arachidonic acid.
Conclusion: These findings, together with evidence from other studies, provide a strong rationale for omega-3 supplementation for patients with liver disease.
Study Quote:"One of the most important findings of our study was that increased intake of omega-3-polyunsaturated fatty acids inhibited the formation of eicosanoids
Links:
Ana González-Périz, Raquel Horrillo, Natàlia Ferré, Karsten Gronert, Baiyan Dong, Eva Morán-Salvador, Esther Titos, Marcos Martínez-Clemente, Marta López-Parra, Vicente Arroyo, and Joan Clària.
-3 fatty acids: a role for resolvins and protectinsFurther Reading (Full Text Sources):
Hasturk H et al. ,
Resolvin E1 Regulates Inflammation at the Cellular and Tissue Level and Restores Tissue Homeostasis In Vivo. J Immunol 2007 179: 7021-7029
Serhan CN et al.
Resolution of inflammation: state of the art, definitions and terms FASEB J. (2007)21: 325-332.













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