Actions and comparative efficacy of phosphatidylcholine formulation and isolated sodium deoxycholate for different...

Phosphatidylcholine formulation has been used to dissolve local fat deposits. This study aimed to evaluate and compare the effects of phosphatidylcholine formulation and its vehicle sodium deoxycholate alone on different cell lines to understand better its mechanism of action.

Cells and media including 3T3-L1 preadipocytes, normal foreskin fibroblasts, neonatal human dermal microvascular endothelial cells (CADMEC), and fetal human skeletal muscle cells (HSkMC) were used. After 24 h, cells were exposed in 3-4, 5-dimethylthiazol-2-yl-2, 3-diphenyl tetrazolium bromide reagent (MTT assays) to increasing dosages of phosphatidylcholine formulation (0.0156-0.5 mg/ml) or an equivalent vehicle, sodium deoxycholate solution, pH 9.0 (0.0066-0.210 mg/ml). Viability was assessed after 1, 2, and 3 days of treatment. Fat tissue (4 x 4 cm) obtained ex vivo from the dorsal fat pads of five rabbits was injected with 2 ml of phosphatidylcholine formulation (50 mg/ml), sodium deoxycholate (21 mg/ml), or normal saline and incubated for 24 h. These were examined histologically to identify cell lysis and morphologic changes.

At 0.125- and 0.25-mg/ml doses of phosphatidylcholine solution, CADMEC and HSkMC were more sensitive (P < 0.001, one-way ANOVA) than adipocytes at all time points examined. Phosphatidylcholine formulation at a dose of 0.5 mg/ml and the equivalent vehicle, sodium deoxycholate, at a dose of 0.21-mg/ml both induced nearly 100% fat cell lysis after 24 h, and evidence of cell lysis as early as 6 h after exposure. After incubation of fat tissue for 24 h with phosphatidylcholine formulation, loss of intracellular lipid staining with an increase in extracellular lipids was seen.

Isolated sodium deoxycholate was almost as effective as the phosphatidylcholine formulation, at clinical concentrations, in reducing the viability of mature adipocytes over time. Similar cytotoxic effects of phosphatidylcholine formulation on normal foreskin fibroblasts, endothelial cells, and human skeletal muscle cells also were observed. The data prove that the formulation acts in a nonspecific manner and that its unintentional administration to other tissues causes cell death.