Disrupted adipokine secretion and inflammatory responses in human adipocyte hypertrophy

Adipocyte hypertrophy is a critical contributor to obesity-induced inflammation and insulin resistance. This study employed a human adipocyte hypertrophy model to investigate the adipokine release, inflammatory responses, and the intracellular singling pathways. Hypertrophic adipocytes exhibited increased lipid content and lipolysis, a decline of anti-inflammatory adipokine adiponectin release and an increase of pro-inflammatory adipokine leptin release compared to mature adipocytes. Moreover, TNFα and LPS exacerbated the decrease in adiponectin secretion by hypertrophic adipocytes while promoting the secretion of leptin, MCP-1 and IL-6, which is associated with impaired activation of p38 and JNK MAPK and persistent activation of ERK and IκBα in hypertrophic adipocytes. These altered adipokine secretions and inflammatory responses within hypertrophic adipocytes may contribute to adipocyte dysfunction in human obesity.