Two scientists at Baylor College of Medicine, Drs. Kjersti Aagaard and Melissa Suter, took a unique approach to looking at the fetal origins of metabolic syndrome, which includes conditions such as obesity, diabetes, and heart disease. Whereas other researchers focus solely on the diets of mothers before and after birth, the BCM researchers were interested in the paternal component of metabolic syndrome.
Published in American Journal of Obstetrics and Gynecology, the study used wild type female mice receiving a normal or high-fat diet for two weeks before mating and throughout breast feeding. These mice were mated with male mice with only one copy of the gene Glut4. Offspring consequently had one or two copies of Glut4, and the offspring with only one copy were predisposed to metabolic syndrome.
Testing of the offspring at birth and five weeks later revealed different fetal liver epigenetic markings as a result of different histone activity in the high-fat group. Whether or not the offspring had one or two copies of Glut4 made no difference, and the epigenetic changes persisted to the five-week point. “More than 200 genes underwent this epigenetic marking,” said Dr. Aagaard in a news release.
Dr. Suter explained the paternal contribution: “When we looked at the wild type versus the Glut4 mice, it showed that the dad’s contribution along with that of the mom changed the fetal epigenome.” Dr. Aagaard said, “This is really a good model system to look at Dad’s contribution. We are finding innovative ways to understand genetic susceptibility, which can, to a large extent, dictate what epigenetic variations can and cannot occur. We are looking at the attributable risk of an exposure in utero versus the additional contribution of the genomic variations and the exposure itself.”
Other researchers involved in the effort include Jun Ma and Alan Harris of BCM and Patricia M. Vuguin, Kirsten Hartil, Ariana Fiallo and Maureen Charron of Albert Einstein College of Medicine in New York.