Picard Frédéric, Géhin Martine, Annicotte Jean- Sébastien, Rocchi Stéphane, Champy Marie-France, O'Malley Bert W, Chambon Pierre, Auwerx Johan
Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, 67404 Illkirch, France.
Cell. 2002 Dec 27;111(7):931-41. doi: 10.1016/s0092-8674(02)01169-8.
We have explored the effects of two members of the p160 coregulator family on energy homeostasis. TIF2-/- mice are protected against obesity and display enhanced adaptive thermogenesis, whereas SRC-1-/- mice are prone to obesity due to reduced energy expenditure. In white adipose tissue, lack of TIF2 decreases PPARgamma activity and reduces fat accumulation, whereas in brown adipose tissue it facilitates the interaction between SRC-1 and PGC-1alpha, which induces PGC-1alpha's thermogenic activity. Interestingly, a high-fat diet increases the TIF2/SRC-1 expression ratio, which may contribute to weight gain. These results reveal that the relative level of TIF2/SRC-1 can modulate energy metabolism.
我们探究了p160辅调节因子家族的两个成员对能量平衡的影响。TIF2基因敲除小鼠对肥胖具有抗性,且适应性产热增强,而SRC-1基因敲除小鼠则因能量消耗减少而易于肥胖。在白色脂肪组织中,TIF2的缺失会降低PPARγ活性并减少脂肪堆积,而在棕色脂肪组织中,它会促进SRC-1与PGC-1α之间的相互作用,从而诱导PGC-1α的产热活性。有趣的是,高脂饮食会增加TIF2/SRC-1的表达比率,这可能导致体重增加。这些结果表明,TIF2/SRC-1的相对水平能够调节能量代谢。