Project
Galactose and Intestinal metabolic health
Prolonged breastfeeding is recommended by the WHO to support proper development and prevent diseases in young children. In this project we will use a preclinical mouse model to gain in-depth knowledge about the role of the intestines in the health-promoting effects of galactose on metabolic health. This knowledge can be applied in further human research that may be especially important in infants and toddlers, potentially inhibiting or even preventing the development of metabolic diseases later in life.
Background
Metabolic diseases pose an increasing burden on health and economics worldwide. Therefore, preventive measures that reduce and delay the onset of these diseases must be extensively investigated. For example, nutritional interventions starting in infancy can be a successful strategy to prevent later‐life dysfunctions, such as obesity and associated diabetes. After birth, critical time points in the offspring’s development include lactation, weaning, and early post weaning. Nutrition, and particularly breastfeeding, during these periods plays a major role, with short‐ and long-term beneficial health implications. In this context, dietary galactose, a monosaccharide naturally present in milk as part of lactose, has been shown to have beneficial effects on fat mass gain, hepatic health, and insulin resistance. However, little is known about how galactose affects intestinal health and whether changes in intestinal homeostasis are responsible for the previously observed systemic positive effects of galactose.
Project description
In this project, we conduct several mouse studies in which young mice will be isocalorically fed either a galactose containing diet, a lactose containing diet, or a control diet. We aim to determine how (ga)lactose affects metabolic health and more specifically intestinal health, by studying its molecular effects on the intestinal inflammation, intestinal barrier function, and the microbiome, and its connection to liver and adipose tissue. To achieve this, we are performing gene and protein expression analysis with physiological measurements like
non‐invasive indirect calorimetry. Based on these new insights, our project will contribute to the development of nutrition‐based approaches to prevent metabolic diseases in the short‐ and long‐term.
Results
Intestinal energy metabolism can be modulated by galactose intake. Galactose increases mitochondrial gene expression, especially mitochondrial OXPHOS related genes. Intestinal galactose modulation of energy metabolism is linked to hepatic health