Around the world, the prevalence of obesity is increasing relentlessly. Once obesity is acquired, weight loss is difficult to achieve and in particular to maintain. Furthermore, the prevalence of obesity in children and young adults is also increasing and more strongly associated with obesity-related morbidities than in older populations. The origins of obesity are first evident in utero, as the fetal response to parental nutritional status. Studies in animals have shown how acquired parental obesity can be transmitted across generations via epigenetic mechanisms through either maternal or paternal gametes. Human studies to investigate whether similar epigenetic mechanisms associated with periconception paternal obesity and insulin resistance might also influence fetal growth are of great scientific interest. Our aim is to generate a robust ‘obesity-associated’ DNA methylation profile (DMP) and validation of genomic regions selected from previous studies of adult obesity, insulin resistance, metabolic syndromes, and fetal growth retardation. We will do this by examining the epigenetic pattern in peripheral blood samples from men either above 30 in BMI or below 25. If we find differences we will extend the data analyses to full trios (mother, father and child).
