Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Difference between revisions of "Chabi 2016 Exp Gerontol"

From Bioblast
(Created page with "{{Publication |title=Chabi B, Pauly M, Carillon J, Carnac G, Favier FB, Fouret G, Bonafos B, Vanterpool F, Vernus B, Coudray C, Feillet-Coudray C, Bonnieu Z, Lacan D, Koechlin-Ra...")
Β 
Line 1: Line 1:
{{Publication
{{Publication
|title=Chabi B, Pauly M, Carillon J, Carnac G, Favier FB, Fouret G, Bonafos B, Vanterpool F, Vernus B, Coudray C, Feillet-Coudray C, Bonnieu Z, Lacan D, Koechlin-Ramonatxo C (2016) Protective effect of myostatin gene deletion on aging-related muscle metabolic decline. Exp Gerontol 78:23-31. Β 
|title=Chabi B, Pauly M, Carillon J, Carnac G, Favier FB, Fouret G, Bonafos B, Vanterpool F, Vernus B, Coudray C, Feillet-Coudray C, Bonnieu Z, Lacan D, Koechlin-Ramonatxo C (2016) Protective effect of myostatin gene deletion on aging-related muscle metabolic decline. Exp Gerontol 78:23-31.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/26944368 PMID: 26944368]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/26944368 PMID: 26944368]
|authors=Chabi B, Pauly M, Carillon J, Carnac G, Favier FB, Fouret G, Bonafos B, Vanterpool F, Vernus B, Coudray C, Feillet-Coudray C, Bonnieu Z, Lacan D, Koechlin-Ramonatxo C
|authors=Chabi B, Pauly M, Carillon J, Carnac G, Favier FB, Fouret G, Bonafos B, Vanterpool F, Vernus B, Coudray C, Feillet-Coudray C, Bonnieu Z, Lacan D, Koechlin-Ramonatxo C
Line 7: Line 7:
|abstract=While myostatin gene deletion is a promising therapy to fight muscle loss during aging, this approach induces also skeletal muscle metabolic changes such as mitochondrial deficits, redox alteration and increased fatigability. In the present study, we evaluated the effects of aging on these features in aged wild-type (WT) and mstn knockout (KO) mice. Moreover, to determine whether an enriched-antioxidant diet may be useful to prevent age-related disorders, we orally administered to the two genotypes a melon concentrate rich in superoxide dismutase for 12 weeks. We reported that mitochondrial functional abnormalities persisted (decreased state 3 and 4 of respiration; p<0.05) in skeletal muscle from aged KO mice; however, differences with WT mice were attenuated at old age in line with reduced difference on running endurance between the two genotypes. Interestingly, we showed an increase in glutathione levels, associated with lower lipid peroxidation levels in KO muscle. Enriched antioxidant diet reduced the aging-related negative effects on maximal aerobic velocity and running limit time (p<0.05) in both groups, with systemic adaptations on body weight. The redox status and the hypertrophic phenotype appeared to be beneficial to KO mice, mitigating the effect of aging on the skeletal muscle metabolic remodeling.
|abstract=While myostatin gene deletion is a promising therapy to fight muscle loss during aging, this approach induces also skeletal muscle metabolic changes such as mitochondrial deficits, redox alteration and increased fatigability. In the present study, we evaluated the effects of aging on these features in aged wild-type (WT) and mstn knockout (KO) mice. Moreover, to determine whether an enriched-antioxidant diet may be useful to prevent age-related disorders, we orally administered to the two genotypes a melon concentrate rich in superoxide dismutase for 12 weeks. We reported that mitochondrial functional abnormalities persisted (decreased state 3 and 4 of respiration; p<0.05) in skeletal muscle from aged KO mice; however, differences with WT mice were attenuated at old age in line with reduced difference on running endurance between the two genotypes. Interestingly, we showed an increase in glutathione levels, associated with lower lipid peroxidation levels in KO muscle. Enriched antioxidant diet reduced the aging-related negative effects on maximal aerobic velocity and running limit time (p<0.05) in both groups, with systemic adaptations on body weight. The redox status and the hypertrophic phenotype appeared to be beneficial to KO mice, mitigating the effect of aging on the skeletal muscle metabolic remodeling.
|keywords=Antioxidant, GDF-8 deletion, Respiratory control ratio, Running capacity, SODB
|keywords=Antioxidant, GDF-8 deletion, Respiratory control ratio, Running capacity, SODB
|mipnetlab=FR Montpellier Wrutniak-Cabello
}}
}}
{{Labeling
{{Labeling

Revision as of 14:49, 9 May 2016

Publications in the MiPMap
Chabi B, Pauly M, Carillon J, Carnac G, Favier FB, Fouret G, Bonafos B, Vanterpool F, Vernus B, Coudray C, Feillet-Coudray C, Bonnieu Z, Lacan D, Koechlin-Ramonatxo C (2016) Protective effect of myostatin gene deletion on aging-related muscle metabolic decline. Exp Gerontol 78:23-31.

Β» PMID: 26944368

Chabi B, Pauly M, Carillon J, Carnac G, Favier FB, Fouret G, Bonafos B, Vanterpool F, Vernus B, Coudray C, Feillet-Coudray C, Bonnieu Z, Lacan D, Koechlin-Ramonatxo C (2016) Exp Gerontol

Abstract: While myostatin gene deletion is a promising therapy to fight muscle loss during aging, this approach induces also skeletal muscle metabolic changes such as mitochondrial deficits, redox alteration and increased fatigability. In the present study, we evaluated the effects of aging on these features in aged wild-type (WT) and mstn knockout (KO) mice. Moreover, to determine whether an enriched-antioxidant diet may be useful to prevent age-related disorders, we orally administered to the two genotypes a melon concentrate rich in superoxide dismutase for 12 weeks. We reported that mitochondrial functional abnormalities persisted (decreased state 3 and 4 of respiration; p<0.05) in skeletal muscle from aged KO mice; however, differences with WT mice were attenuated at old age in line with reduced difference on running endurance between the two genotypes. Interestingly, we showed an increase in glutathione levels, associated with lower lipid peroxidation levels in KO muscle. Enriched antioxidant diet reduced the aging-related negative effects on maximal aerobic velocity and running limit time (p<0.05) in both groups, with systemic adaptations on body weight. The redox status and the hypertrophic phenotype appeared to be beneficial to KO mice, mitigating the effect of aging on the skeletal muscle metabolic remodeling. β€’ Keywords: Antioxidant, GDF-8 deletion, Respiratory control ratio, Running capacity, SODB

β€’ O2k-Network Lab: FR Montpellier Wrutniak-Cabello


Labels: MiParea: Respiration, Genetic knockout;overexpression, Exercise physiology;nutrition;life style  Pathology: Aging;senescence 

Organism: Mouse  Tissue;cell: Skeletal muscle  Preparation: Isolated mitochondria  Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III 

Coupling state: LEAK, OXPHOS 

HRR: Oxygraph-2k 

Labels, 2016-05