Boss O, Samec S, Desplanches D, Mayet M H, Seydoux J, Muzzin P, Giacobino J P
Department of Medical Biochemistry, Faculty of Medicine, University of Geneva, Switzerland.
FASEB J. 1998 Mar;12(3):335-9. doi: 10.1096/fasebj.12.3.335.
Endurance exercise training has been shown to decrease diet-induced thermogenesis (DIT) in rats and humans. In rodents, most thermogenesis is thought to occur in brown adipose tissue via activation of the uncoupling protein-1 (UCP1) and in skeletal muscle. Since the level of UCP1 mRNA in rat BAT was reported to be unmodified by exercise training, the newly described uncoupling proteins UCP2 and UCP3 could be responsible for the decreased DIT in trained rats. UCP3 mRNA levels in endurance-trained rats were found to be reduced by 76% and 59% in tibialis anterior and soleus muscles, respectively. UCP2 mRNA levels were also decreased in tibialis anterior and in heart by 54% and 41%, respectively. Neither white adipose tissue UCP2 nor brown adipose tissue UCP1, UCP2, and UCP3 mRNA levels were modified. The results of this study show that a need for a higher metabolic efficiency is associated with decreased mRNA expression of the uncoupling proteins in skeletal and heart muscles, which would decrease energy dissipation in these tissues. The down-regulation of UCP3 and UCP2 expressions might also contribute to the rapid weight gain known to occur when exercise training ceased.
耐力运动训练已被证明会降低大鼠和人类的饮食诱导产热(DIT)。在啮齿动物中,大多数产热被认为是通过解偶联蛋白-1(UCP1)的激活在棕色脂肪组织以及骨骼肌中发生。由于据报道运动训练不会改变大鼠棕色脂肪组织中UCP1 mRNA的水平,新发现的解偶联蛋白UCP2和UCP3可能是训练大鼠DIT降低的原因。在耐力训练的大鼠中,发现胫骨前肌和比目鱼肌中UCP3 mRNA水平分别降低了76%和59%。胫骨前肌和心脏中UCP2 mRNA水平也分别降低了54%和41%。白色脂肪组织UCP2以及棕色脂肪组织UCP1、UCP2和UCP3的mRNA水平均未改变。这项研究的结果表明,对更高代谢效率的需求与骨骼肌和心肌中解偶联蛋白的mRNA表达降低有关,这会减少这些组织中的能量消耗。UCP3和UCP2表达的下调也可能导致运动训练停止时出现的快速体重增加。