The number of obese women in the childbearing age is drastically increasing globally. As a consequence, more children are born by obese mothers. Unfortunately, maternal obesity and/ or high fat intake during pregnancy increase the risk of developing obesity, type-2 diabetes, cardiovascular disease and non-alcoholic fatty liver disease in the children, which passes obesity and metabolic dysfunction on from generation to generation. Several studies try to elucidate causative effects of maternal metabolic markers on the metabolic imprinting in the children; however diet induced obesity is also associated with chronic low grade inflammation. Nobody have yet investigated the role of this inflammatory phenotype, but here we demonst rate that obesity induced inflammation is reversed during pregnancy in mice, and is therefore less likely to affect the fetal programming of metabolic dysfunction. Instead, we suggest that an early elevated lipid exposure caused by a maternal high fat feeding might be more important for long term metabolic imprinting in the offspring. Therefore, we study the effect of maternal high fat/high sucrose diet during gestation, lactation or both to elucidate if perinatal adaptations to a high fat/high sucrose diet makes the offspring more capable of dealing with a high fat diet later in life. We demonstrate that a dietary mismatch between pre- and post-natal life alters the phenotype in an obese prone rat model at weaning. Thus, exposure to a control diet in utero and a high fat/high sucrose diet during lactation cause more severe phenotypic alteration in the offspring at weaning than pups exposed to the high fat/high sucrose diet both in utero and during lactation. The same pattern is seen in the adult offspring after being challenged with a high fat diet for 6 weeks. However HFHS exposure during fetal life protected against hyperleptinemia in the adult off spring during the challenge. Additionally, offspring expose to high fat/high sucrose diet during lactation displayed a decrease level of inflammatory genes in the blood, which could indicated that perinatal HFHS exposure protect against the detrimental effects of high fat feeding leading to metabolic disease.