Enterococcus faecalis is an opportunistic pathogen. Similarly, to other pathogens that have been historically regarded as exclusively extracellular, E. faecalis has the ability to adhere to, enter, persist and divide in a wide range of mammalian cells. However, the mechanisms that support the intracellular growth of E. faecalis are not yet established. Here, we show that inhibition of the host lipid droplets (LDs) biogenesis impairs intracellular bacterial growth. We also show that E. faecalis infection induces a transient decrease in LD levels, which is prolonged in the absence of CodY, a global regulatory protein that regulates genes involved in metabolism and virulence in response to nutrient availability. The deletion of codY enhances intracellular growth in hepatocytes, and triglycerides and glycerol utilization in vitro. Together, we propose that the glycerol present in the triglycerides stored in the LDs may be catabolized via the glpk and dhaK pathways. These findings illustrate the importance of host lipid metabolism in supporting E. faecalis intracellular growth, and they emphasize the regulatory role of CodY in balancing nutrient acquisition and intracellular multiplication. This study paves the way for understanding the mechanisms of cellular infection by E. faecalis and the consequences of this lifestyle on the host.