Lipin, a lipodystrophy and obesity gene
Lipin, a lipodystrophy and obesity gene
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DOI：
10.1016/j.cmet.2004.12.002
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发表时间：
2005-01-01
期刊：
影响因子：
29
通讯作者：
Reue, K
中科院分区：
文献类型：
--
作者：
Phan, J;Reue, K
脂肪代谢障碍和肥胖症代表了肥胖症谱的极端和相反的两端，并且通常归因于不同基因组的表达或功能的改变。我们以前证明，脂蛋白缺乏损害脂肪细胞分化，并导致脂质代谢障碍的小鼠。使用两种不同的组织特异性脂蛋白转基因小鼠品系，我们现在证明，增强脂肪组织或骨骼肌中的脂蛋白表达促进肥胖。这通过两种组织中的不同机制发生，脂肪组织中的脂蛋白水平影响脂肪细胞的脂肪储存能力，骨骼肌中的脂蛋白水平作为全身能量消耗和脂肪利用的决定因素。因此，单独的脂蛋白水平的变化足以诱导肥胖的极端状态，并且可能代表脂肪组织和骨骼肌调节脂肪质量和能量平衡的机制。
Lipodystrophy and obesity represent extreme and opposite ends of the adiposity spectrum and have typically been attributed to alterations in the expression or function of distinct sets of genes. We previously demonstrated that lipin deficiency impairs adipocyte differentiation and causes lipodystrophy in the mouse. Using two different tissue-specific lipin transgenic mouse strains, we now demonstrate that enhanced lipin expression in either adipose tissue or skeletal muscle promotes obesity. This occurs through diverse mechanisms in the two tissues, with lipin levels in adipose tissue influencing the fat storage capacity of the adipocyte, and lipin levels in skeletal muscle acting as a determinant of whole-body energy expenditure and fat utilization. Thus, variations in lipin levels alone are sufficient to induce extreme states of adiposity and may represent a mechanism by which adipose tissue and skeletal muscle modulate fat mass and energy balance.