Finck Brian N, Gropler Matthew C, Chen Zhouji, Leone Teresa C, Croce Michelle A, Harris Thurl E, Lawrence John C, Kelly Daniel P
Center for Cardiovascular Research and Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Cell Metab. 2006 Sep;4(3):199-210. doi: 10.1016/j.cmet.2006.08.005.
Perturbations in hepatic lipid homeostasis are linked to the development of obesity-related steatohepatitis. Mutations in the gene encoding lipin 1 cause hepatic steatosis in fld mice, a genetic model of lipodystrophy. However, the molecular function of lipin 1 is unclear. Herein, we demonstrate that the expression of lipin 1 is induced by peroxisome proliferator-activated receptor gamma (PPARgamma) coactivator 1alpha (PGC-1alpha), a transcriptional coactivator controlling several key hepatic metabolic pathways. Gain-of-function and loss-of-function strategies demonstrated that lipin selectively activates a subset of PGC-1alpha target pathways, including fatty acid oxidation and mitochondrial oxidative phosphorylation, while suppressing the lipogenic program and lowering circulating lipid levels. Lipin activates mitochondrial fatty acid oxidative metabolism by inducing expression of the nuclear receptor PPARalpha, a known PGC-1alpha target, and via direct physical interactions with PPARalpha and PGC-1alpha. These results identify lipin 1 as a selective physiological amplifier of the PGC-1alpha/PPARalpha-mediated control of hepatic lipid metabolism.
肝脏脂质稳态的紊乱与肥胖相关脂肪性肝炎的发生有关。编码脂联素1的基因突变会在fld小鼠(一种脂肪营养不良的遗传模型)中导致肝脏脂肪变性。然而,脂联素1的分子功能尚不清楚。在此,我们证明脂联素1的表达由过氧化物酶体增殖物激活受体γ(PPARγ)共激活因子1α(PGC-1α)诱导,PGC-1α是一种控制多个关键肝脏代谢途径的转录共激活因子。功能获得和功能丧失策略表明,脂联素选择性激活PGC-1α靶途径的一个子集,包括脂肪酸氧化和线粒体氧化磷酸化,同时抑制脂肪生成程序并降低循环脂质水平。脂联素通过诱导核受体PPARα(一种已知的PGC-1α靶标)的表达,并通过与PPARα和PGC-1α的直接物理相互作用,激活线粒体脂肪酸氧化代谢。这些结果确定脂联素1是PGC-1α/PPARα介导的肝脏脂质代谢控制的选择性生理放大器。