Schrauwen P, Walder K, Ravussin E
Clinical Diabetes and Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix AZ 85016, USA.
Obes Res. 1999 Jan;7(1):97-105. doi: 10.1002/j.1550-8528.1999.tb00396.x.
Uncoupling protein (UCP) 2 and UCP3 are newly discovered proteins that can uncouple ATP production from mitochondrial respiration, thereby dissipating energy as heat and affecting energy metabolism efficiency. In contrast to UCP1, which is only present in brown adipose tissue, UCP2 has a wide tissue distribution, whereas UCP3 is expressed predominantly in skeletal muscle. Some evidence of a role for UCPs in modulating metabolic rate was provided by linkage and association studies. Furthermore, UCP3 gene expression was found to correlate negatively with body mass index and positively with sleeping metabolic rate in Pima Indians. Treatment with thyroid hormone increases expression of the UCP2 and UCP3 genes. Other regulators of UCP2 and UCP3 gene expression are beta3-adrenergic agonists and glucocorticoids. Surprisingly, fasting has a stimulatory effect on UCP2 and UCP3 mRNA levels, possibly explained by the effects of free fatty acid on UCP2 and UCP3 gene expression.
解偶联蛋白（UCP）2和UCP3是新发现的蛋白，它们可使ATP生成与线粒体呼吸解偶联，从而将能量以热量形式耗散，并影响能量代谢效率。与仅存在于棕色脂肪组织中的UCP1不同，UCP2具有广泛的组织分布，而UCP3主要在骨骼肌中表达。连锁和关联研究提供了一些关于UCP在调节代谢率中作用的证据。此外，在皮马印第安人中发现UCP3基因表达与体重指数呈负相关，与睡眠代谢率呈正相关。甲状腺激素治疗可增加UCP2和UCP3基因的表达。UCP2和UCP3基因表达的其他调节因子是β3 - 肾上腺素能激动剂和糖皮质激素。令人惊讶的是，禁食对UCP2和UCP3 mRNA水平有刺激作用，这可能由游离脂肪酸对UCP2和UCP3基因表达的影响来解释。
