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

Autor(es)

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]

Afiliação do(s) autor(es)

^[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

• Tipo de documento: Artigo Científico
• Fonte: PLoS One; v. 8, n. 10 OCT 4 2013.
• Citações Web of Science: 21

Resumo

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)

• Processo FAPESP: 12/13071-0 - Bases celulares do efeito anti-atrófico de leucina no músculo esquelético: papel de VPS34
• Beneficiário: Igor Luchini Baptista
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 07/57613-3 - Efeitos celulares e moleculares da sobrecarga de leucina na atrofia muscular induzida pelo desuso
• Beneficiário: Igor Luchini Baptista
• Modalidade de apoio: Bolsas no Brasil - Doutorado Direto
• Processo FAPESP: 06/61523-7 - Aspectos celulares e moleculares da plasticidade muscular
• Beneficiário: Anselmo Sigari Moriscot
• Modalidade de apoio: Auxílio à Pesquisa - Temático