| Summary: | 碩士 === 國立暨南國際大學 === 生物醫學科技研究所 === 97 === Obesity is strongly associated with the development of cardiovascular diseases and type 2 diabetes mellitus. Adipocytes are not only an energy reservoir but also endocrine cells, which can secrete a variety of bioactive molecules called adipokines, and play crucial role in regulation of energy balance and metabolism. Recent studies suggest that macrophages can infiltrate into adipose tissues, and cause adipose tissue dysfunction. To address the effect of insulin on the biological functions of adipocyte, an established cell model, differentiated 3T3-L1 adipocytes were used. Additionally, the effects of macrophage secreted factors on the expression of adipokines and cytokines in both untreated and insulin-treated 3T3-L1 cells were also examined. Our results showed that treatment with high insulin or high insulin plus high glucose could significantly increase TNF-α, IL-6, MCP-1, adiponectin and leptin production, as well as fatty acid accumulation. Co-culture of 3T3-L1 adipocytes with macrophage conditioned-medium and insulin caused a significantly increase of IL-6 and MCP-1 production, but decrease of adiponectin production. Peroxisome proliferator-activated receptor-γ (PPAR-γ) regulates adipocyte genes involved in adipogenesis and lipid metabolism. 3T3-L1 adipocytes cultured with macrophage conditioned medium resulted in decrease of PPARγ expression, with subsequent reduction of fatty acid synthase production. These findings indicated that certain macrophage-secreted molecules might induce adipocyte-mediated inflammation, and obesity not only induces insulin resistance and type 2 diabetes mellitus, but also provokes serious inflammatory reactions. The established adipocyte cell model can be used to examine the obesity, lipogenesis and metabolism related studies. Besides, this model also can be used as a platform to screen therapeutic drugs for treatment of diabetes mellitus.
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