Ricquier D
Centre de Recherche sur l'Endocrinologie Moléculaire et le Développement, 92190 Meudon Cedex, France.
Curr Opin Drug Discov Devel. 1999 Sep;2(5):497-504.
The mechanisms explaining the imperfect coupling of respiration to ADP phosphorylation in mitochondria are not well understood. In the case of a thermogenic organ such as brown adipose tissue, heat production results from a regulated uncoupling of respiration due to a specific uncoupler present in the inner mitochondrial uncoupling protein, referred to as uncoupling protein (UCP)-1. UCP1 functions as a proton translocator regulated by fatty acids. Two UCP homologues were identified very recently; UCP2 is expressed in most organs, whereas UCP3 expression is restricted to skeletal muscle and brown adipose tissue. Experimental data support the respiration uncoupling activity of UCP2 and UCP3. Physiological and genetic data are in agreement with thermogenic activity of the two proteins, although other physiological data favor a role for UCP2 and UCP3 in lipid handling rather than in energy expenditure. UCP2 and UCP3 may also be involved in inflammation, immune response and fever. Many hormones and certain pharmacological regulators affect expression level of UCP2 and/or UCP3 gene.
线粒体中呼吸作用与ADP磷酸化之间耦合不完善的机制尚未完全明确。在诸如棕色脂肪组织这样的产热器官中，热量产生源于呼吸作用的调节性解偶联，这是由于线粒体内膜存在一种特定的解偶联剂，即解偶联蛋白（UCP）-1。UCP1作为一种受脂肪酸调节的质子转运体发挥作用。最近发现了两种UCP同源物；UCP2在大多数器官中表达，而UCP3的表达仅限于骨骼肌和棕色脂肪组织。实验数据支持UCP2和UCP3的呼吸解偶联活性。生理和遗传数据与这两种蛋白质的产热活性一致，尽管其他生理数据表明UCP2和UCP3在脂质处理而非能量消耗方面发挥作用。UCP2和UCP3也可能参与炎症、免疫反应和发热。许多激素和某些药理调节剂会影响UCP2和/或UCP3基因的表达水平。
