|Title:||Potential involvement of dietary advanced glycation end products in impairment of skeletal muscle growth and muscle contractile function in mice|
|Authors:||Egawa, Tatsuro https://orcid.org/0000-0001-9363-1589 (unconfirmed)|
Hayashi, Tatsuya https://orcid.org/0000-0001-7600-4735 (unconfirmed)
|Author's alias:||江川, 達郎|
Muscle fatigue resistance
Muscle force production
|Publisher:||Cambridge University Press (CUP)|
|Journal title:||British Journal of Nutrition|
|Abstract:||Diets enriched with advanced glycation end products (AGE) have recently been related to muscle dysfunction processes. However, it remains unclear whether long-term exposure to an AGE-enriched diet impacts physiological characteristics of skeletal muscles. Therefore, we explored the differences in skeletal muscle mass, contractile function and molecular responses between mice receiving a diet high in AGE (H-AGE) and low in AGE (L-AGE) for 16 weeks. There were no significant differences between L-AGE and H-AGE mice with regard to body weight, food intake or epididymal fat pad weight. However, extensor digitorum longus (EDL) and plantaris (PLA) muscle weights in H-AGE mice were lower compared with L-AGE mice. Higher levels of N[ε] -(carboxymethyl)-l-lysine, a marker for AGE, in EDL muscles of H-AGE mice were observed compared with L-AGE mice. H-AGE mice showed lower muscle strength and endurance in vivo and lower muscle force production of PLA muscle in vitro. mRNA expression levels of myogenic factors including myogenic factor 5 and myogenic differentiation in EDL muscle were lower in H-AGE mice compared with L-AGE mice. The phosphorylation status of 70-kDa ribosomal protein S6 kinase Thr, an indicator of protein synthesis signalling, was lower in EDL muscle of H-AGE mice than that of L-AGE mice. These findings suggest that long-term exposure to an AGE-enriched diet impairs skeletal muscle growth and muscle contractile function, and that these muscle dysfunctions may be attributed to the inhibition of myogenic potential and protein synthesis.|
|Rights:||© The Authors 2017|
The full-text file will be made open to the public on 1 January 2018 in accordance with publisher's 'Terms and Conditions for Self-Archiving'.
|Appears in Collections:||Journal Articles|
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.