High level of uncoupling protein 1 expression in muscle of transgenic mice selectively affects muscles at rest and decreases their IIb fiber content
| Autor: | Anne-Marie Cassard-Doulcier, Daniel Ricquier, Frédéric Bouillaud, Christophe Fleury, Elodie Couplan, Susanne Klaus, Marc Goubern, A. Xavier Bigard, Maria-del-Mar Gonzalez-Barroso, Philippe Mateo, Philippe Diolez, C. Gelly, Mathieu Silberberg, Catherine de Montrion, Michel Lonchampt, Eric Thiaudière, Silvia Ortmann, Bruno Quesson, Nigel Levens |
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| Rok vydání: | 2002 |
| Předmět: |
medicine.medical_specialty
Phosphocreatine Rest Mice Transgenic Mitochondrion Biology Biochemistry Ion Channels Mitochondrial Proteins Mice Adenosine Triphosphate Adipose Tissue Brown Internal medicine Brown adipose tissue medicine Uncoupling protein Animals Glycolysis Muscle Skeletal Molecular Biology Uncoupling Protein 1 Soleus muscle Membrane potential Body Weight Skeletal muscle Membrane Proteins Heart Cell Biology Myocardial Contraction Thermogenin Mitochondria Mitochondria Muscle Rats Endocrinology medicine.anatomical_structure Phenotype Organ Specificity Muscle Fibers Fast-Twitch Regression Analysis Carrier Proteins Energy Intake Energy Metabolism |
| Zdroj: | The Journal of biological chemistry. 277(45) |
| ISSN: | 0021-9258 |
| Popis: | The mitochondrial uncoupling protein of brown adipose tissue (UCP1) was expressed in skeletal muscle and heart of transgenic mice at levels comparable with the amount found in brown adipose tissue mitochondria. These transgenic mice have a lower body weight, and when related to body weight, food intake and energy expenditure are increased. A specific reduction of muscle mass was observed but varied according to the contractile activity of muscles. Heart and soleus muscle are unaffected, indicating that muscles undergoing regular contractions, and therefore with a continuous mitochondrial ATP production, are protected. In contrast, the gastrocnemius and plantaris muscles showed a severely reduced mass and a fast to slow shift in fiber types promoting mainly IIa and IIx fibers at the expense of fastest and glycolytic type IIb fibers. These observations are interpreted as a consequence of the strong potential dependence of the UCP1 protonophoric activity, which ensures a negligible proton leak at the membrane potential observed when mitochondrial ATP production is intense. Therefore UCP1 is not deleterious for an intense mitochondrial ATP production and this explains the tolerance of the heart to a high expression level of UCP1. In muscles at rest, where ATP production is low, the rise in membrane potential enhances UCP1 activity. The proton return through UCP1 mimics the effect of a sustained ATP production, permanently lowering mitochondrial membrane potential. This very likely constitutes the origin of the signal leading to the transition in fiber types at rest. |
| Databáze: | OpenAIRE |
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