On the basis of the above findings it may be concluded that although placental transfer of lipids is small, sustained maternal hyperlipidemia during late gestation is of pivotal importance for the metabolism of the mother and her offspring. Besides aporting essential metabolites to the fetus in an indirect manner, such as glucose synthesized in maternal liver from glycerol released from adipose tissue, the active lipidic metabolism in the mother allows the availability of high amounts of circulating triglyceride-rich lipoproteins for milk synthesis in preparation for lactation. The induction of LPL activity in the mammary gland is important for this function, and warrants the availability of essential fatty acids from the diet to be present in the milk, as well as contributes to the disappearance of maternal hyperlipidemia around parturition. Besides, maternal hyperlipidemia constitutes a floating energetic store to be used under conditions of food deprivation to ensure the availability of alternative substrates for maternal tissues, such a ketone bodies, and to save essential metabolites for the fetus. Maternal hyperlipidemia is the result of numerous and dynamic metabolic adaptations that have to be controlled very finely. Any deviation from this control may alter maternal lipoprotein profile and even be responsible for an alteration in the milk composition, as it has been already reported in dyslipidemic mothers .