Phosphatidylcholine causes adipocyte-specific lipolysis and apoptosis in adipose and muscle tissues

Abstract

Phosphatidylcholine (PPC) formula has been therapeutically used to reduce areas of localized fat. However, no single research has been carried out on its effect on a variety of cells in adipose and muscle tissues. Herein, the current study aimed to explore the activity of PPC on different cells in adipose and muscle tissues and to investigate the molecular mechanisms contributing to the effects of PPC on lipolysis and apoptosis. mRNA expression levels of various genes were measured by quantitative real-time PCR. Protein expression levels were observed through Western blotting and cell viability was measured by MTT assay. Lipolysis and caspase 3 activity assay were performed using commercial kits. PPC induces lipolysis and apoptosis in adipocytes (3T3-L1), but not in the other tested cells, including skeletal muscle cells (C2C12 myocytes), endothelial cells (HUVEC), and fibroblasts (BJ). The possible role of TNF alpha and IL-1 beta-mediated pathways on the effects of PPC was also revealed. We confirmed that treatment with PPC caused lipolysis and apoptosis in a dose-dependent manner (only in 3T3-L1 adipocytes). The effect of PPC observed in 3T3-L1 adipocytes was not evident in C2C12 myocytes, HUVEC, and fibroblasts. PPC also increased TNFa and IL-1 beta expression and release in 3T3-L1 adipocytes in a dose-dependent fashion, but not in C2C12 myocytes, HUVEC, and BJ. Suppression of TNF alpha or IL-1 beta reversed PPC-induced lipolysis and apoptosis in 3T3-L1 adipocytes, suggesting that PPC could promote adipocyte-specific lipolysis and apoptosis through TNF alpha and IL-1 beta-mediated signaling. We conclude that the specific activity of PPC on adipocyte in adipose without other tissue damages can be an effective approach for melting lipid.