Skeletal muscle mitochondrial oxidative capacity and uncoupling protein 3 are differently influenced by semistarvation and refeeding

FEBS Letters

Dulloo, A.G¹  Montani, J.P¹  Solinas, G¹  Mainieri, D¹  Crescenzo, R¹  Iossa, S³  Liverini, G³  Seydoux, J² 

[1] Department of Medicine, Division of Physiology, University of Fribourg, Chemin du Musée 5, 1700 Fribourg, Switzerland;Department of Physiology, Faculty of Medicine, University of Geneva, Geneva, Switzerland;Department of General and Environmental Physiology, University of Naples ‘Federico II’, Naples, Italy

关键词: Obesity;    Cachexia;    Thermogenesis;    UCP3;    Mitochondrial energetics;    UCP3;    uncoupling protein 3;    MOC;    mitochondrial oxidative capacity;    ATP;    adenosine triphosphate;    ADP;    adenosine diphosphate;   

DOI  :  10.1016/S0014-5793(03)00491-5

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

We investigated, in skeletal muscle mitochondria isolated from semistarved and refed rats, the relation between the protein expression of uncoupling protein 3 (UCP3) and mitochondrial oxidative capacity, assessed as state 4 and state 3 respiration rates in presence of substrates that are either non-lipids (glutamate, succinate) or lipids (palmitoyl CoA, palmitoylcarnitine). During semistarvation, when whole-body thermogenesis is diminished, state 3 respiration was lower than in fed controls by about 30% independently of substrate types, while state 4 respiration was lower by 20% only during succinate oxidation, but UCP3 was unaltered. After 5 days of refeeding, when thermogenesis is still diminished, neither state 4, state 3 nor UCP3 were lower than in controls. Refeeding on a high-fat diet, which exacerbates the suppression of thermogenesis, resulted in a two-fold elevation in UCP3 but no change in state 4 or state 3 respiration. These results during semistarvation and refeeding, in line with those previously reported for fasting, are not in support of the hypothesis that UCP3 is a mediator of adaptive thermogenesis pertaining to weight regulation, and underscore the need for caution in interpreting parallel changes in UCP3 and mitochondrial oxidative capacity as the reflection of mitochondrial uncoupling by UCP3.

【 授权许可】

Unknown