肥満マウスの肝臓および脂肪組織におけるＢＤＮＦおよびその受容体ＴｒｋＢの発現変化

抄録

Brain derived neurotrophic factor (BDNF) has been known as a critical player of neural development, synaptic plasticity and potential rescue factor for neuronal disorders. However, recent studies suggest that BDNF has other potential regulatory role in peripheral tissues: for example, BDNF regulates immune functions through the high affinity receptor of BDNF, TrkB, in some immune tissues and cells. Here we report that BDNF and TrkB-T1, the truncated form of TrkB, also express in white adipose tissue (WAT) and the liver in mice and that the expression dramatically changes in obese mice. In lean C57/BL6 mice, BDNF expressed in the liver but not WAT, while TrkB-T1 expressed in WAT but not the liver. In leptin deficient-obese mice (ob/ob), the expression of BDNF dramatically increased in WAT, whereas the expression of TrkB-T1 increased in the liver. Treatment of lean mice with high fat diet also increased their expression in WAT and the liver. Fractionation of WAT with collagenase revealed that BDNF and TrkB-T1 express in mature adipocytes but not in vascular and other types of cells in WAT. We also found that 3T3-L1 adipocyte expresses BDNF and TrkB-T1. BDNF increased the phosphorylation of Akt, p44/42 MAPK and transcriptional factor FKHR in 3T3-L1 adipocyte. Furthermore, BDNF significantly decreased the gene expression of the atherosclerogenic adipokine PAI-1 in the cells. These results suggest that BDNF and TrkB-T1 play a role in the regulation of metabolism in the liver and WAT in lean and obese mice. [J Physiol Sci. 2007;57 Suppl:S182]