Prenatal development may adopt unique patterns of metabolic responses to different nutrient supplies. AMPK and mTOR are two central metabolic regulators, with AMPK acting to slow down and mTOR to promote anabolism. Here, we observed surprisingly that mTORC1 in the foetal liver remains active in low glucose, although AMPK is effectively activated in an AMP-dependent manner. Mechanistically, we found that TRPV4, one main member of TRPVs in the liver, is acetylated, disabling its inactivation by FBP-unoccupied aldolase. It suggested that the TRPV-mediated resistance of mTORC1 inhibition in low glucose for normal foetal development.