According to scientists from Washington University School of Medicine in St. Louis, specific forms of the additive may one day find themselves added to foods not to act as emulsifiers but to control blood lipids and reduce risk for diabetes, hypertension or cardiovascular disease.
Lecithin appears to work by binding with a protein in the liver called PPAR-alpha, known to play a role in lipid and glucose metabolism, according to results published yesterday in Cell.
Current pharmaceutical approaches to lower triglyceride levels and elevate good cholesterol in the blood work by activating PPAR-alpha, said the researchers, led by Irfan Lodhi.
Lecithin was originally made from egg yolk, but is now more commonly made from plants and vegetables, most notably soybeans. As an emulsifier, it plays an important part in obtaining the right texture for a variety of applications, including chocolate and confectionery, margarines and spreads, bakery, beverages, convenience foods, processed meats and ice cream.
"By identifying this substance that occurs naturally in the body - and also happens to be used as a food additive - it may be possible to improve the [management] of lipid disorders and minimize drug side effects by adding particular varieties of lecithin to food,” said Dr Lodhi.
By using mice that could not make fatty acid synthase in the liver, and then treating them with fibrate drugs, the researchers showed that PPAR-alpha was activated. The lipid levels of the mice subsequently returned to normal levels, leading the scientists to “suspect that fatty acid synthase also was involved in the activation of PPAR-alpha”, said senior investigator Clay Semenkovich.
The enzyme and the protein had never been connected due to the location of each: PPAR-alpha is a nuclear receptor situated in the nucleus of the cell, while fatty acid synthase is found in the cytoplasm.
According to the Missouri-based researchers the fatty compounds called phosphatidylcholines contained with lecithin produce the effect. Mass spectrometry and gene expression studies were employed to isolate the phosphatidylcholine that activated PPAR-alpha in the liver.
“That information could be used […] to develop what people sometimes refer to as nutriceuticals,” said Semenkovich.
Published online ahead of print, 30 July 2009, doi: 10.1016/j.cell.2009.05.036
“Identification of a Physiologically Relevant Endogenous Ligand for PPAR-alpha in Liver”
Authors: M.V. Chakravarthy, I.J. Lodhi, L. Yin, R.R.V. Malapaka, H.E. Xu, J. Turk, C.F. Semenkovich