The influx of extracellular Ca2+ is implicated in various functions of white fat adipocytes which include glucose utilization, lipolysis and adipokine secretion. Consequently dysregulation of Ca2+ influx may be involved in the aetiology of the metabolic syndrome. Since little is known about Ca2+ entry pathways in these cells we have addressed this question using Ca2+ imaging and molecular biology methods on rat epididymal adipocytes. Data is quoted as medians with 95% confidence intervals. Under basal conditions the intracellular calcium concentration, [Ca2+]i was 130 nM (124-138; n=466). In 42 cells tested, removal of extra Ca2+ reversibly decreased this by of 18% (11-27). 20µM verapamil and 20µM nifedipine, blockers of L-type calcium channels, both mimicked the effect of Ca2+ removal and prevented Ca2+ entry and recovery of basal [Ca2+]i when added just before the re-addition of extracellular Ca2+ following its removal. These effects were not shared by 10µM KBR-7943, a blocker of Na+-Ca2+ exchange. RT-PCR indicated the presence of mRNA for CaV3.2, CaV1.1, CaV1.2 and CaV1.3, however Western blots of the membrane fraction only revealed the presence of CaV1.3 alpha-subunit. In conclusion our data suggests that a background window Ca2+ current through CaV1.3 maintains [Ca2+]i in white fat adipocytes; this idea compatible and consistent with their depolarized membrane potential (-30mV, Bentley et al 2014) at which this channel type is expected to be open as well as a previous molecular study that also demonstrates the presence of L-type Ca2+ channels in this cell type (Gaur et al 1988).