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Title: Potential involvement of dietary advanced glycation end products in impairment of skeletal muscle growth and muscle contractile function in mice
Authors: Egawa, Tatsuro  kyouindb  KAKEN_id
Tsuda, Satoshi
Goto, Ayumi
Ohno, Yoshitaka
Yokoyama, Shingo
Goto, Katsumasa
Hayashi, Tatsuya  kyouindb  KAKEN_id
Author's alias: 江川, 達郎
Keywords: Muscle strength
Muscle fatigue resistance
Muscle force production
Myogenesis
Protein synthesis
Issue Date: Jan-2017
Publisher: Cambridge University Press (CUP)
Journal title: British Journal of Nutrition
Volume: 117
Start page: 21
End page: 29
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[389], 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'.
URI: http://hdl.handle.net/2433/225061
DOI(Published Version): 10.1017/S0007114516004591
Appears in Collections:Journal Articles

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