Brand Martin D, Esteves Telma C
MRC Dunn Human Nutrition Unit, Hills Road, Cambridge, United Kingdom.
Cell Metab. 2005 Aug;2(2):85-93. doi: 10.1016/j.cmet.2005.06.002.
Evidence for the physiological functions of UCP2 and UCP3 is critically reviewed. They do not mediate adaptive thermogenesis, but they may be significantly thermogenic under specific pharmacological conditions. There is strong evidence that the mild regulated uncoupling they cause attenuates mitochondrial ROS production, protects against cellular damage, and diminishes insulin secretion. Evidence that they export fatty acids physiologically is weak. UCP2 and UCP3 are important potential targets for treatment of aging, degenerative diseases, diabetes, and perhaps obesity.
对UCP2和UCP3生理功能的证据进行了严格审查。它们不介导适应性产热,但在特定药理条件下可能具有显著的产热作用。有强有力的证据表明,它们引起的轻度调节性解偶联可减弱线粒体活性氧的产生,防止细胞损伤,并减少胰岛素分泌。关于它们在生理状态下输出脂肪酸的证据不足。UCP2和UCP3是治疗衰老、退行性疾病、糖尿病以及或许还有肥胖症的重要潜在靶点。