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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Leucine and HMB Differentially Modulate Proteasome System in Skeletal Muscle under Different Sarcopenic Conditions

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Baptista, Igor L. [1] ; Silva, Willian J. [1] ; Artioli, Guilherme G. [2] ; Guilherme, Joao Paulo L. F. [2] ; Leal, Marcelo L. [1] ; Aoki, Marcelo S. [3] ; Miyabara, Elen H. [1] ; Moriscot, Anselmo S. [1]
Total Authors: 8
[1] Univ Sao Paulo, Dept Anat, Inst Biomed Sci, Sao Paulo - Brazil
[2] Univ Sao Paulo, Sch Phys Educ & Sport, Sao Paulo - Brazil
[3] Univ Sao Paulo, Sch Arts Sci & Humanities EACH, Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: PLoS One; v. 8, n. 10 OCT 4 2013.
Web of Science Citations: 21

In the present study we have compared the effects of leucine supplementation and its metabolite beta-hydroxy-beta-methyl butyrate (HMB) on the ubiquitin-proteasome system and the PI3K/Akt pathway during two distinct atrophic conditions, hindlimb immobilization and dexamethasone treatment. Leucine supplementation was able to minimize the reduction in rat soleus mass driven by immobilization. On the other hand, leucine supplementation was unable to provide protection against soleus mass loss in dexamethasone treated rats. Interestingly, HMB supplementation was unable to provide protection against mass loss in all treatments. While solely fiber type I cross sectional area (CSA) was protected in immobilized soleus of leucine-supplemented rats, none of the fiber types were protected by leucine supplementation in rats under dexamethasone treatment. In addition and in line with muscle mass results, HMB treatment did not attenuate CSA decrease in all fiber types against either immobilization or dexamethasone treatment. While leucine supplementation was able to minimize increased expression of both Mafbx/Atrogin and MuRF1 in immobilized rats, leucine was only able to minimize Mafbx/Atrogin in dexamethasone treated rats. In contrast, HMB was unable to restrain the increase in those atrogenes in immobilized rats, but in dexamethasone treated rats, HMB minimized increased expression of Mafbx/Atrogin. The amount of ubiquitinated proteins, as expected, was increased in immobilized and dexamethasone treated rats and only leucine was able to block this increase in immobilized rats but not in dexamethasone treated rats. Leucine supplementation maintained soleus tetanic peak force in immobilized rats at normal level. On the other hand, HMB treatment failed to maintain tetanic peak force regardless of treatment. The present data suggested that the anti-atrophic effects of leucine are not mediated by its metabolite HMB. (AU)

FAPESP's process: 12/13071-0 - Cellular bases of the anti-atrophic effects of leucine in the skeletal muscle: role of VPS34
Grantee:Igor Luchini Baptista
Support type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 06/61523-7 - Cellular and molecular aspects of muscular plasticity
Grantee:Anselmo Sigari Moriscot
Support type: Research Projects - Thematic Grants