Early life nutritional metabolic programming for later life metabolic health – the nutritional power of galactose

Obesity has become a worldwide problem. Nutritional interventions can be a promising strategy to delay or even stop development of metabolic diseases. Galactose, if condensed to glucose via ß1,4 glycosidic linkage forms lactose, is an important source of energy in milk for proper mammalian development. Partial replacement of glucose by galactose in post-weaning diets, thus mimicking lactose, is suggested to protect female mice from high fat diet (HFD) induced obesity. It’s however still not clear whether partial replacement of glucose by galactose has the same nutritional (programming) power as lactose. Besides, galactose-induced dose-response effects are also not yet elucidated. Therefore, we hypothesize that partial replacement of glucose by galactose has the same nutritional power as lactose while excluding lactose-intolerant dysfunction, and a different ratio of galactose and glucose in post-weaning diets might lead to different metabolic outcomes. In this project, preclinical animal studies will be conducted to test our hypothesis and elucidate mechanisms underlying the beneficial effects at the physiological, metabolic, and molecular level.