A group of Belgian researchers has determined that a pregnant woman's ability to metabolize fats is determined not only by her genes but by her baby's genes as well. The details of their findings appear in the November issue of the Journal of Lipid Research, an American Society for Biochemistry and Molecular Biology journal.
The researchers, led by Olivier S. Descamps of the Centre de Recherche Médicale de Jolimont in Haine Saint-Paul and of the Université Catholique de Louvain in Brussels, studied genes and proteins involved in fat metabolism from the blood and placenta of 525 pregnant women. Because all cells from the placenta originate from the fetus, they are a good indication of the genes and proteins produced by the baby.
Descamps and his co-workers discovered that the baby's genes had almost as much influence as the mother's genes on her lipoprotein levels. Because increased levels of lipoproteins can lead to pre-eclampsia and pancreatitis in pregnant women and also increase their future risk of cardiovascular disease, these findings are of particular interest to the medical community.
"The lipoprotein particle is composed of proteins called apolipoproteins and lipids such as cholesterol and triglycerides." explains Descamps. "Lipoproteins represent the only way for lipids, which are insoluble in water, to be transported through the blood circulation, composed exclusively of water."
The study focused on two specific proteins involved in lipid metabolism, lipoprotein lipase and apolipoprotein E. "Apolipoprotein E and lipoprotein lipase play important roles in the degradation of triglyceride-rich lipoproteins," notes Descamps. "In pregnant women, the concentrations of these lipoproteins are particularly very high and it is thought that these lipoproteins are the forms that carry the lipids to the placenta.
The researchers looked at several genetic variations (also known as polymorphisms) of lipoprotein lipase and apolipoprotein E that are known to influence the concentrations of triglycerides and cholesterol in the general population. They found that when these polymorphisms were present in the babies, their mothers' triglyceride and cholesterol levels were influenced to the same extent that they would be if the polymorphisms were present in the mothers. However, when both the mother and fetus expressed the same polymorphism, the results were not always as predicted. For example, a genetic variation that raises the levels of triglycerides and cholesterol when expressed in mothers may lower these levels when it is expressed simultaneously by the fetus in the placenta.
These findings have implications for many women who are advised not to have children due to genetic defects in lipoprotein metabolism. Because their fetuses can compensate for their defects, the women may actually be able to bear children without complications.
The American Society for Biochemistry and Molecular Biology (ASBMB) is a nonprofit scientific and educational organization with over 11,000 members in the United States and internationally. Most members teach and conduct research at colleges and universities. Others conduct research in various government laboratories, nonprofit research institutions, and industry.
Founded in 1906, the Society is based in Bethesda, Maryland, on the campus of the Federation of American Societies for Experimental Biology. The Society's primary purpose is to advance the sciences of biochemistry and molecular biology through its publications, the Journal of Biological Chemistry, the Journal of Lipid Research, Molecular and Cellular Proteomics, and Biochemistry and Molecular Biology Education, and the holding of scientific meetings.
For more information about ASBMB, see the Society's website at www.asbmb.org.
The manuscript for the Journal of Lipid Research paper can be downloaded from the following URL: http://www.jlr.org/cgi/content/abstract/M500223-JLR200
The above post is reprinted from materials provided by American Society for Biochemistry and Molecular Biology. Note: Materials may be edited for content and length.
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