Circulating triglycerides (TGs) in the parental circulation are metabolized into FFAs by lipases like lipoprotein lipase (LPL) at the placenta. The FFAs are able to be transported into placental cells by a variety of fatty acid transport proteins (FATP), fatty acid translocase (FAT/CD36), and plasma membrane-bound fatty acid binding proteins (FABPpm), alongside other crucial fuels like glucose in response to physiologic alterations in insulin and plasma lipids in pregnancy. Intracellular fatty acid binding proteins (FABP3 and 5) shuttle fatty acids toward incorporation into phospholipids or toward energy production through β-oxidation in the mitochondria (facilitated by the carnitine shuttle system's CPT1a and CPT2). Triacylglycerols (TAG) and well as phospholipids like phosphatidylcholine (PC) are synthesized within the placenta for their storage as lipid droplets, facilitated by PLIN2/adipophilin (ADRP), and their mobilization to be transported into fetal circulation. Acyl-transferase enzymes like glycerol-3-phosphate acyltransferase (GPAT) and 1-acylglycerol-3-phosphate-O-acyltransferases (AGPAT2 and AGPAT4) in the Kennedy Pathway and phospholipase A2 (PLA2G4c) and lysophosphatidylcholine acyltransferase (LPCAT4) in the Lands’ cycle remodel the fatty acid species being transported to the fetus. These elements of lipid metabolism in the placenta can be studied over gestation as well as between control and obese pregnancies to determine the mechanisms driving this important element of fuel transport, as demonstrated by Bidne et al. [23] in this issue of Clinical Science. Created with BioRender.com.