Study Finds Mechamism for How Omega-3 Fats Help Blood Sugar HealthBy

Greg Arnold, DC, CSCS, September 30, 2010, abstracted from “GPR120 Is an Omega-3 Fatty Acid Receptor Mediating Potent Anti-inflammatory and Insulin-Sensitizing Effects” in the September 3, 2010 issue of Cell

Insulin is a hormone released by the pancreas “that is needed to convert sugar, starches, and other food into energy needed for daily life” (1). Over time, consistently high blood sugar levels can cause muscles and organs to become resistant to insulin, causing “insulin resistance” (2). It also significantly increases the risk for diabetes, which affected 23.6 million Americans in 2007 and costs our healthcare system $174 billion each year (3, 4).

In addition to high blood sugar levels, insulin resistance is also caused by chronic inflammation in the body (5). Because of this role in precipitating insulin resistance, interest in using omega-3 fats due to their anti-inflammatory properties to help with insulin resistance has become more popular (6). Now a new study (7) has found a possible mechanism for just how omega-3 fats help control inflammation and maintain normal insulin function.

In the study, researchers took 21 8-week old normal and 14 8-week old mice genetically engineered to have high levels of inflammation, due to a specific protein called GPR120 (8) being deactivated. All mice were fed either a normal diet (13.5% of calories from fat) or a high-fat diet (60% of calories from fat) for 15 weeks. After 15 weeks, 7 mice from each group were then placed on a diet with the same amount of calories, but now containing 16% calories from EPA and 9% of calories from DHA, both omega-3 fats, a diet that has been used in previous research (9). The omega-3 diet was followed for 5 weeks. Finally, 7 more mice were taken from the regular group at 15 weeks and given a popular insulin resistance drug, Rosiglitazone (Avandia) (10), for 5 weeks to compare to the omega-3 group.

By the end of the study, the researchers found that normal mice put on the omega-3 fat diet had 42% greater insulin sensitivity than the normal mice following the high-fat diet throughout (24 vs. 14 mg/kg/min). What’s more, the omega-3 fat group had insulin sensitivity that was only 12% lower than a prescription drug used for insulin resistance, Rosiglitazone (Avandia) (27 vs. 24 mg/kg/min). In the mice in which GPR120 was deactivated, no changes in insulin sensitivity were found in the omega-3 group, indicating that adding omega-3 compensated for the loss of GPR120.

For the researchers, “GPR120 is a functional omega-3 fatty acid receptor/sensor and mediates potent insulin sensitizing and anti-diabetic effects…which may prove useful in the future development of new therapeutic approaches for the treatment of insulin resistant diseases.”

Greg Arnold is a Chiropractic Physician practicing in Danville, CA. You can contact Dr. Arnold directly by emailing him at PitchingDoc@msn.com or visiting his web site at www.PitchingDoc.com

Reference:

1. “National Diabetes Fact Sheet: Diabetes Definitions” - http://www.cdc.gov/diabetes/pubs/definitions.htm
2. “Insulin Resistance and Pre-Diabetes” - http://www.diabetes.niddk.nih.gov/dm...ance/index.htm
3. “Diabetes Research and Statistics” - http://www.cdc.gov/diabetes/consumer/research.htm
4. “2007 National Diabetes Fact Sheet” - http://www.cdc.gov/diabetes/pubs/estimates07.htm
5. Schenk, S., Saberi, M., and Olef sky, J.M. (2008). Insulin sensit ivity: modulatio n by nutrie nts and infl ammation. J. Clin. In vest. 118 , 2992–30 02.
6. González-Périz A Obesity-induced insulin resistance and hepatic steatosis are alleviated by omega-3 fatty acids: a role for resolvins and protectins. FASEB J. 2009 Jun;23(6):1946-57. Epub 2009 Feb 11.
7. Oh DY. GPR120 Is an Omega-3 Fatty Acid Receptor Mediating Potent A nti-inflammatory and Insulin-Sensitizing Effects. Cell 142, 687–698
8. Gotoh C. The regul ation of adipogenesis thro ugh GPR120. Biochem. Biop hys. Res. Commu n 2007; 354: 591–597.
9. Neschen S. n-3 Fatty acids preserve insulin sensitivity in vivo in a peroxis ome proliferat or-activated receptor-alp ha-dependen t manner. Diabetes 2007; 56: 1034–10 41
10. “Rosiglitazone” - http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001051