An EU-funded research team has discovered that blood vessels and muscles in the heart can regulate the uptake of fatty acids from our diet, and has worked out how they do this. The results, published in the journal Nature, could pave the way for new forms of treatment for fat accumulation in the muscles which can increase the risk of developing type II diabetes and cardiovascular disease. The study was part of the 16-partner EU project LYMPHANGIOGENOMICS ('Genome-wide discovery and functional analysis of novel genes in lymphangiogenesis'), which received EUR 9 million under the 'Life sciences, genomics and biotechnology for health' Thematic area of the Sixth Framework Programme (FP6). We take fatty acids into our bodies through foods such as meat, fish and milk products. Some fatty acids, such as omega 3, which is found in oily fish such as mackerel, salmon, tuna and halibut, can significantly help reduce the risk of both strokes and cardiovascular disease. Previous research had demonstrated that too high a build-up of fatty acids in the muscles can contribute to the development of insulin resistance and consequently type II diabetes, which currently affects around 38 million Europeans. An understanding of how the fatty acid uptake is regulated is therefore imperative to finding ways to control the condition. Up to now, the function of the blood vessels in fatty acid management has not been properly studied, even though fatty acids must be transported through the cells of the vascular walls before metabolism by the muscles begins. The research team studied a protein called VEGF-B (vascular endothelial growth factor B), which signals from the muscles to the blood vessels. They observed a correlation between VEGF-B levels and the mitochondrial content and energy levels of the muscles. They also saw that the protein can control the level of FATPs (fatty acid transport proteins) in the vascular walls. Associate Professor Ulf Eriksson, who led the team at the Department of Medical Biochemistry and Biophysics at the Karolinska Institutet in Sweden said, 'Mice that lacked either the VEGF-B protein or its receptors in the walls of the blood vessels had a lower intake of fat to the muscles and the heart, and less accumulation of fat in the different tissues. Instead, we found that the residual fat accumulated in the white adipose tissue, causing a slight weight increase in the mice.' However, the most important finding, from the point of view of diabetes research, was that the mice lacking the VEGF-B protein (that therefore had a lower uptake of muscular fat) had a higher uptake of sugar to the heart. Insulin resistance, reduced uptake of sugar to the muscles and high blood glucose levels are the main indications of type II diabetes. Therefore, the project's results offer new insights for the development of new treatments for type II diabetes and several other metabolic diseases. 'There's a well-known correlation between fat accumulation in muscle tissue and insulin resistance and adult diabetes,' noted Professor Eriksson. 'We are now making rigorous efforts to examine how we can affect insulin signalling and reduce the level of blood glucose in diabetic mice by blocking VEGF-B signalling.' Also involved in the study were researchers from Uppsala University, Gothenburg University and the Sahlgrenska University Hospital, all in Sweden, and the University of Kuopio in Finland.