Researchers from Massachusetts General Hospital (MGH) have found that tissues from mice transgenic for a gene usually found in the c.elegans roundworm contain omega-3 fatty acids, consumption of which has been shown to protect against heart disease. Usually mammals cannot produce omega-3s from the more abundant omega-6 fatty acids, which do not have the health benefits of omega-3s. The finding, published in the February 5 issue of Nature, could lead to development of omega-3-rich meat, milk and eggs.

Many studies have confirmed that consumption of omega-3s can reduce the incidence and effects of cardiovascular disease for both the general public and those with existing disease. The American Heart Association currently recommends consumption of two or more weekly servings of fish, particularly fatty fish like trout and salmon, which are naturally high in omega 3s.

"Correction of the usually omega-3-deficient Western diet has become a key step toward reducing the risk of several modern diseases," says lead author Jing X. Kang, MD, PhD, of the MGH Department of Medicine. "The current approach to increasing omega-3s in animal food products is to feed livestock with fish meal or other marine products, which is time consuming, costly and limited by the availability of those feeds."

Investigating a potential novel way further to increase omega-3 consumption, the MGH researchers developed a strain of mice that have the c. elegans gene fat-1, which codes for an enzyme that converts omega-6 acids to omega-3s. The transgenic mice appeared perfectly healthy and were raised, along with normal mice, on a diet low in omega-3s.

Tissues from the transgenic mice were found to be high in omega-3 fatty acids, while the tissues from normal mice had fats primarily consisting of omega-6s, as do most mammals. The ability to transmit fat-1 into mammals without losing its effectiveness or causing any apparent harm to the transgenic animals raise
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Contact: Sue McGreevey
smcgreevey@partners.org
617-724-2764
Massachusetts General Hospital
4-Feb-2004

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