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Current research shows that low-grade, chronic inflammation in your body — specifically your fat cells — could be one cause for the rise in obesity. Low grade inflammation in your adipose tissue has been linked to altered fat metabolism, plus the secretion and release of pro-inflammatory cytokines that further aggravate inflammation levels in your body. It has been shown that a high-fat diet could induce an environment that harbors inflammation, therefore worsening the overall conditions associated with dysfunctional fat cells, as well as extra fat being stored in your liver. Current and past research has shown that the omega-3 fatty acids (DHA and EPA) may be effective at combating high-fat induced diets, therefore lowering inflammation and potentially improving health.

In fact, a study published in Diabetologia, could show a link between omega-3 fatty acids intake and reduced inflammation in white adipose tissue (fat cells).

Let me explain…

Inflammation and Fat Cells

It has been shown that inflammation in your fat cells reduces adipokines that are responsible for normal energy and fat metabolism.

It has also been shown that there could be a down-regulation of these powerful adipokines, and an increase in pro-inflammatory cytokines, therefore increased inflammation.

However, it has been shown that a high-fat diet, mainly comprised of omega-3 fatty acids, may be beneficial at reducing inflammation, therefore potentially increasing the expression of adiponectin from your fat cells. The authors of this study wanted to determine if a high omega-3 fatty acid diet could positively affect white adipose tissue (fat cell) inflammation and gene expression in obese, diabetic mice.

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They fed obese diabetic mice and lean diabetic-free mice one of four diets: a standard low-fat diet, a high-fat diet comprised of saturated and monounsaturated fats, a high-fat diet comprised of omega-6 fatty acids, and a high-fat diet comprised of omega-3 fatty acids. The researchers noted that a high, saturated-fat diet increased the genes responsible for inflammation when compared to the standard low-fat diet. They also showed there was increased macrophages invasion into fat cells in the high saturated-fat group. They did note that there was a small increase in inflammation associated with the high omega-6 fat group.

The researchers showed that a high-omega-3 fat diet completely prevented macrophage invasion into fat cells which is normally seen in a high-fat induced diet, despite no change in the bodyweight of the mice. They also showed that most high-fat diets down regulated the expression and plasma concentration of adiponectin, however, they did note this was not the case in the omega-3 fatty acids group.

From their work, they concluded that omega-3 fatty acids may prevent adipose tissue inflammation that could be caused by a high-fat diet. Their data also suggested that beneficial effects of omega-3 fatty acids on diabetes development could be caused by their effects on adipose tissue inflammation. Although more research needs to be completed to verify their findings, this could strengthen the argument that omega-3 fatty acids, when part of a healthy diet, could reduce fat cell inflammation and may stimulate the expression and secretion of weight management adipokines.

Omega-3 Fatty Acids and Your Weight

Omega-3 fatty acids have been shown beneficial in many different aspects of health. However, as it pertains to this article, omega-3 fatty acids could reduce or prevent inflammation of your fat cells, which could increase your risk for chronic disease development.

Including a diet rich in omega-3 fatty acids may lead to overall better health, reduced inflammation, improved heart health, and may increase natural fat-burning hormones naturally secreted by your fat cell



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Todoric J, Loffler M, Huber J, Bilban M, Reimers M, Kadl A, Zeyda M, Waldhaust W, Slulnig TM. Adipose tissue inflammation induced by a high-fat diet in obese diabetic mice is prevented by n-3 polyunsaturated fatty acids. Diabetologia. 2006 Sep;49(9):2109–19. Epub 2006 Jun 17.

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