At our request, omega-3 expert Joyce Nettleton, D.Sc., presents several reports on the fatty acid science summit in London, where the world's leading researchers presented new findings 
by Joyce A. Nettleton, D.Sc. 

Elsewhere in this issue of Vital Choices, you'll find photos from the two omega-3 science conferences we attended in Europe last month (See “Vital Choice Salmon Serves Top Omega-3 Scientists”).
Both were attended by the world's leading fatty acid research scientists, and featured a wealth of new findings and insights.
The first, called “A Celebration of DHA,” was convened at the Royal Society of Medicine in London, while the second took place in the Netherlands.
We asked expert attendee Joyce Nettleton, D.Sc., to summarize the presentations that addressed various topics, including brain, heart, and metabolic health.
Dr. Nettleton is a widely published expert on omega-3 science and seafood health-nutrition topics. She issues regular fatty acid science updates in her great Fats of Life (consumer-oriented) and PUFA (scientist-oriented) e-newsletters.
Tonight, we present the first of these reports, focused on omega-3s' apparent or potential impacts on weight control and metabolic health, with implications for diabetes.
Polyunsaturated fats, metabolism and diabetes
An exclusive report on omega-3 research from the 2010 Masstricht meeting of the International Society for Study of Fats & Lipids (ISSFAL)
By Joyce A. Nettleton, D.Sc.
The pre-diabetic condition known as metabolic syndrome (MetS) is a cluster of abnormalities that place people at very high risk of developing adult (type 2) diabetes.
The abnormalities that combine to define MetS include:
  • High blood pressure
  • Excess abdominal fat
  • High triglyceride (fat) levels
  • Sticky blood (platelet activation)
  • Low levels of HDL (“good”) cholesterol
  • Insulin resistance and/or glucose intolerance (impaired ability to process sugars)
Of these signs, the key characteristic of MetS is insulin resistance… a weakened response to insulin… the hormone that allows cells to absorb blood sugar (glucose) to burn for energy.
The rapid increase in the number of people with MetS and diabetes parallels the high rates of obesity observed in the last 20 years, although MetS can occur without obesity.
It has long been thought that abnormalities in lipid (fat and cholesterol) metabolism promote the bodily processes associated with MetS and diabetes.
In particular, people with MetS or diabetes are less able to oxidize or “burn” fatty acids, thus contributing to the deposition of fat in the liver and skeletal muscle (Hoeks J, 2010).
Presentations at the May 2010 meeting of ISSFAL (International Society for the Study of Fatty Acids and Lipids) supported this concept.
Omega-3 Fatty Acids May Improve Insulin Resistance
Recent animal studies suggest that the high levels of free fatty acids observed in MetS and diabetes undermine the cells' energy-producing machinery, the mitochondria (Goodpaster B, 2010, Mittra S et al., 2008).
However, with EPA from fish oil, mitochondrial function and the oxidation of fatty acids and glucose improved (Rustan A, 2010; Fiamoncini J et al., 2010; Nemoto N et al., 2009).
Others have reported that omega-3 fatty acids reduced the development of obesity-related insulin resistance (Gonzalez-Periz A et al., 2009).
These effects contributed to lower fat accumulation and better glucose tolerance.
Another ISSFAL presentation reported that a fish oil diet reduced the secretion of cholesterol from the liver and improved impaired “insulin signaling” in rats with abnormal blood lipid profiles and MetS (Borthwick F et al., 2010).
EPA or a fish oil diet also affects the genes involved in fat and energy metabolism (Rustan A, 2010). Those involved in energy utilization and fatty acid oxidation are turned up, while those governing fat production and deposition are turned down.
Interestingly, French researchers reported that animals genetically predisposed to obesity fed a diet rich in alpha-linolenic acid, the plant-based omega-3 fatty acid, tolerated glucose better at lower insulin levels compared with lean animals fed a control diet (Fevre C et al., 2010).
The obese, alpha-linolenic-fed animals also had improved insulin signaling that resulted in better insulin sensitivity.
Whether these effects were attributable to alpha-linolenic itself, or the long-chain omega-3s made from it, is not known.
Editor's Note: Stay tuned for Dr. Nettleton's next report, “Do Omega-6 Fatty Acids Promote Fat Accumulation?”
  • Borthwick F, Lu J, Hassanali Z, et al. Dietary n-3 PUFA improves post-prandial metabolism in the insulin resistant JCR:LA-cp rat by lowering enterocytic apoB48 production and lymphatic cholesterol. Abstract. ISSFAL 2010, Maastricht, Netherlands. P 55.
  • Fevre C, Bellenger S, Narce M, et al. Effects of α-linolenic acid enriched diet on metabolic syndrome: improvement of liver insulin resistance by modulating insulin signaling pathway. Poster. ISSFAL 2010, Maastricht, Netherlands. P 79.
  • Gonzalez-Periz A, Horrillo R, Ferré N, et al. Obesity-induced insulin resistance and hepatic steatosis are alleviated by omega-3 fatty acids: a role for resolvins and protectins. FASEB J. 2009;23:1946-1957.
  • Goodpaster B. The role of mitochondria in lipid-induced insulin resistance within skeletal muscle. Abstract. ISSFAL 2010, Maastricht, Netherlands. P 48.
  • Hoeks J. Prolonged fasting-induced insulin resistance, lipid accumulation and mitochondrial dysfunction in human skeletal muscle. Abstract. ISSFAL 2010, Maastricht, Netherlands. P 48.
  • Mittra S, Bansal VS, Bhatnagar PK. From a glucocentric to a lipocentric approach towards metabolic syndrome. Drug Discov Today 2008;13:211-218.
  • Nemoto N,Suzuki S, Kikuchi H, et al. Ethyl-eicosapentaenoic acid reduces liver lipids and lowers plasma levels of lipids in mice fed a high-fat diet. In Vivo 2009;23:685-689.
  • Rustan A. The impact of eicosapentaenoic acid (EPA) on regulation of fatty acid metabolism, metabolic flexibility and gene expression in human skeletal muscle cells. Abstract. ISSFAL 2010, Maastricht, Netherlands. P 59.