| Summary: | 碩士 === 國防醫學院 === 生理學研究所 === 104 === Obesity is a worldwide public health issues. Body energy metabolism is an important cause of obesity and metabolic disease and aging. Growth arrest- specific 6 (Gas6) is a vitamin K-dependent protein, which binding with TAM receptor (Axl, Tyro-3, Mer). Gas6 was also found to be involved in mediating adipocyte survival and proliferation in vitro, which is essential to complete developing into mature adipocytes. The past study shows the expression of plasma Gas6 was significantly higher in obese adolescents. Gas6 deficient mice decrease the accumulation of adipose tissue, and Axl antagonist reduced lipid uptake. In this study we investigate a diet-induced obese rat animal model and preadipocyte cell model, to clarify the role of adipocyte Gas6. The body weight and adipose tissue weight were higher in 6 and 12 weeks HFD group, but food intake were similar among experimental groups. The weight of the Epi and Sub adipose tissues were increased in rats fed a HFD. Significantly higher gene expression of Gas6 and its receptor Axl, were observed in Sub in 12 weeks HFD compared with NCD rats. No significant trend were observed for other receptor Mer and Tyro-3 for 12 weeks, indicating Axl may be the major Gas6 receptor involved in the development of adipose tissue dysfunction. In preadipocytes cell model, indicating the gene expression of Axl is early than Gas6, and higher Gas6 and Axl expression in differentiation phase. However, the underling mechanisms remain elusive.
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