DHA versus EPA: effects on insulin resistance, fatty liver
Posted Oct 09 2010 12:00am
USDA.gov - Some of America’s most popular fish - salmon and albacore tuna, for example - are rich in healthful essential dietary fats known as omega-3 fatty acids. Ongoing studies by U.S. Department of Agriculture (USDA) chemist Darshan S. Kelley and co-investigators are helping to uncover new details about how these fish-oil components help protect us from chronic diseases.
In an early study with laboratory mice, Kelley and colleagues investigated the interplay of two omega-3 fatty acids from fish oil - DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid) - and a third fatty acid, CLA (the trans-10, cis-12 form of CLA) found in some dietary supplements.
Kelley’s 8-week test with 50 laboratory mice indicated that DHA protected the animals against two harmful side effects of CLA: CLA-induced insulin resistance and CLA-induced non-alcoholic fatty-liver disease. In contrast, EPA offered only partial protection against CLA-induced non-alcoholic fatty liver disease and provided no protection against insulin resistance.
If untreated, insulin resistance can lead to diabetes. An estimated 36 million to 57 million Americans are insulin-resistant. Non-alcoholic fatty liver disease can result in cirrhosis of the liver or liver cancer. The study appeared in a 2007 issue of Metabolic Syndrome and Related Disorders.
One area of interest is DHA’s interaction with a recently discovered hormone known as “adiponectin.” Scientists already know some of the basics: Adiponectin is produced by fat cells in adipose tissue; low levels of adiponectin have been associated with insulin resistance; CLA depletes the adipose tissue in which adiponectin is made; and DHA can restore adipose tissue, thus indirectly increasing adiponectin levels.
Kelley and coinvestigators noted that laboratory mice fed the CLA-plus-DHA feed had higher levels of adiponectin than did the mice that were given the feed that contained CLA but not DHA. Thus, “increasing adiponectin levels may be an important mechanism by which DHA protects against insulin resistance,” says Kelley. “But we need to know more.”
In related work, published in a 2009 article in Current Opinion in Clinical Nutrition and Metabolic Care, Kelley and University of California-Davis graduate student Dawn Fedor reviewed results from several dozen EPA and DHA studies. In their review, the scientists indicate that findings reported in the past decade have been inconsistent in regard to the effects of EPA and DHA on insulin resistance in human volunteers.
Their review underscores the need for new investigations, with larger numbers of volunteers. Kelley, for example, would like to determine whether DHA can improve the ability of adult, pre-diabetic volunteers to use insulin efficiently, and thus help delay onset of diabetes. Such research might reveal more about the mechanisms of action that DHA and EPA use, the sites upon which they act in the human body, and the genes that control these mechanisms.