The obesity epidemic represents a major challenge to our health systems. Women of childbearing age are particularly affected. Overweight and obesity have a multitude of adverse health effects and can lead to chronic liver disease and liver cancer. In addition, maternal obesity is associated with metabolic disorders in children, and an increased rate of childhood cancers. Obesity alters the composition of the gut microbiome, which contributes to the progression of chronic liver disease and is passed on to the next generation. The objective of this thesis is to understand the impact of maternal obesity on the risk of developing chronic liver disease and liver cancer in children, and the role of the microbiome in this context. We have demonstrated, in a mouse model, that maternal obesity leads to profound changes in gene expression in their offspring. We observed that signaling pathways of the innate immune system and the cell cycle are altered, and that genes important for the development of chronic liver diseases are dysregulated. In addition, we found that maternal obesity leads to higher rates of steatosis, fibrosis and inflammation in adult offspring of obese mothers. The offspring of obese mothers also have a significantly higher risk of developing liver tumors. The gut microbiome of offspring of obese mouse mothers is altered and these alterations are retained into adulthood. By restoring a normal microbiome, we were able to normalize the next generation's risk of developing liver cancer. This highlights the key role of the gut microbiome and its alterations in the transmission of liver disease from mother to child, and paves the way for the development of a future therapy.