Metabolic syndrome (MS) is a cluster of related life-style diseases including type 2 diabetes, atherosclerosis and obesity. Genetics and nutrition are predisposing factors, but other key determinants such as problematic events in early life may interact to produce clinical MS. Rodents which develop obesity, hyperglycemia and hyperinsulinemia are common as models for T2D and obesity, while the rabbit and the ApoE knock out mouse have been the most popular models for CVD. However, comparing human patients with herbivorous species is difficult. Pigs, on the other hand, are true monogastric omnivores which absorb, transport and digest lipids in a manner close to humans, easily accept eating a human diet, and develop spontaneous atherosclerosis with a location and morphology similar to humans. While the main lipoprotein class is VLDL in rabbits and HDL in rodents, it is LDL in both pigs and humans. Roughly said, pigs express two different phenotypes in relation to MS: A lean and an obese phenotype. Yucatan and Göttingen minipigs may develop obesity and T2D after high calorie feeding. This is not the case in landrace pigs due to their high endothelial lipase activity due to a long history of selective breeding for lean meat, while Göttingen minipigs have not been subjected to such selection. The genetics behind these breed differences are largely unexplored and provide a unique possibility to investigate the genetic and environmental factors leading to MS.  The clinical manifestations of MS occur in adults, but increasing evidence suggests that they arise in early and maybe even fetal life. Low birth weight and formula feeding are considered predisposing factors. Various fetal inflammatory insults, such as infection with Chlamydia pneumoniae or viruses, acting in concert with genetic and hereditary factors, might initiate the development of these changes and in turn increase the tendency for disease progression after birth. It is difficult to mimic early fetal or childhood events by experimental manipulation unless the experimental animals have a certain size and life span. Pigs have a practical size for experimental procedures and porcine nutrition shows a high degree of similarity with human nutrition. In our group we attempt to develop a MS model in the pig, primarily by induction of early life stress and feeding an MS-inducing diet, while we until now have declined from working with the genetic aspects due to economic restraints.